8

Mutant Genes and Linkages

Margaret C. Green

This chapter presents (1) a list of the named mutant genes of the mouse, (2) a summary of information about known linkages, and (3) a discussion of certain kinds of stocks useful for the studying and maintaining mutants. It is an outgrowth of a chapter entitled Gene and Chromosome Mutations by George D. Snell in the first edition of the Biology of the Laboratory Mouse.

Well over 300 mutant genes occupying more than 250 loci are known in the mouse. These numbers are subject to considerable uncertainty because the information about individual mutants varies in reliability. Many have not been adequately tested for allelism with other similar mutants. Many known to be alleles have not been compared sufficiently to determine whether or not their effects are identical by known criteria. Some well described mutants have become extinct. The choice of mutants to be included in the following list has therefore been somewhat arbitrary. I have tried to include all named mutants that seem likely to be useful, with the exception of apparently identical repeat mutations. I have omitted many of the mutants at the complex T locus and all of the alleles at the histocompatibility loci. The histocompatibility loci are described in detail in Chapter 24.

The list of references is not intended to be complete. References in addition to those listed here and appearing before 1950 may be found in Grüneberg ( 1952). Among papers published after that date I have tried to select those giving access to the previous literature. Useful descriptions of mutants affecting the skeleton may be found in Grüneberg ( 1963) and of mutants affecting the nervous system in Sidman et al. ( 1965).

Mutants discussed in other chapters in this book are so indicated by cross references to the appropriate chapters.

The linkage group if known is given in Roman numerals.

a locus, V, Chapter 21. The agouti locus controls the relative amount and distribution of yellow pigment (phaeomelanin) and black pigment (eumelanin) in the hairs of the coat. Experimental evidence indicates that the genes at this locus act only in the hair follicles. Pigment produced at sites other than the hair follicles is always eumelanin regardless of the genotype at the a locus ( Silvers and Russell, 1955, Markert and Silvers, 1956). Mutations from a to a^t or A^w are very common, but other mutations within the locus appear to be rare. See also MGI.

A^y, yellow, semidominant, Chapters 19, 29. An old mutant of the mouse fancy. All the hair pigment is yellow. Heterozygotes usually become obese and sterile after the first few months. They are more susceptible to several kinds of tumors than normal mice ( Vlahakis and Heston, 1963). Homozygotes die before implantation ( Robertson, 1942) or shortly thereafter with failure of trophoblast giant cell development ( Eaton and Green, 1963). A^y is dominant to all other members of the series in the sense that heterozygotes with all other members are indistinguishable from each other. See also MGI.

A^vy, viable yellow, dominant, Chapter 29. Arose spontaneously in the C3H/HeJ inbred strain. A^vy resembles A^y except that homozygotes are viable and indistinguishable from heterozygotes with lower members of the series. Both homozygotes and heterozygotes show considerable variation in appearance ranging from clear yellow, through mottling with dark patches, to a complete agouti-like coat ( Dickie, 1962a). Homozygotes and heterozygotes tend to become obese, and the degree of obesity is correlated with the amount of yellow in the coat ( Wolff, 1965; Dickie, 1965, personal communication). See also MGI.

A^w, white-bellied agouti. Hairs of back are black with a subapical yellow band, the typical "agouti" pattern. The belly is white or cream. Dominant to A and all lower alleles. See also MGI.

+ or A, agouti. Like A^w except that the belly is dark. Usually regarded as the wild-type allele. See also MGI.

Aⁱ, intermediate agouti. Arose spontaneously in the C57BL/6J strain. Aⁱ/Aⁱ, Aⁱ/ A and Aⁱ/ a^td resemble A^w/-. Aⁱ/ a^t and Aⁱ/ a mice have a dark back and light belly with agouti hairs along the sides ( Dickie, 1962b and personal communication). See also MGI.

a^td, tanoid. Arose spontaneously in the C57BL/6J strain. a^td/a^td, a^td/ a^t, and a^td/ a all have a light belly and a very dark agouti back. A/a^td resembles A^w/- ( Loosli, 1963). See also MGI.

a^t, black and tan. Found by Dunn ( 1928) in a strain obtained from an English fancier. Black back and cream or yellow belly. Recessive to A on back but dominant on belly. A/a^t resembles A^w/-. See also MGI.

a, nonagouti. An old mutant of the mouse fancy. a/a mice are plain black on back and belly, with some yellow hairs on the ears and perineum. See also MGI.

a^e, extreme nonagouti. Found among descendants of an irradiated mouse ( Hollander and Gowen, 1956). a^e/a^e mice are very dark all over with no yellow hairs in the ears or around the nipples and perineum. Recessive to all other alleles. See also MGI.

a^x, radiation-induced, lethal when homozygous. Recessive to A^y, A^w, A, a^t, dominant to a. a^x/ a has lighter belly than a/ a. a^x shows about 0.5 per cent recombination with A^y ( L.B. Russell et al., 1963). See also MGI.

ab, asebia, recessive, linkage not known. Arose as a spontaneous mutation in the BALB/CCrglGa strain. Homozygotes may be recognizable at 7 days of age by retarded growth of the coat. Alopecia increases and at adulthood the hair is very sparse. Sebaceous glands are completely absent. The base of the hair follicles sometimes exhibits excessive development, but hair production is faulty. The centers of many follicles are plugged with keratotic material. The follicles extend deep into the fat tissue and single hair-follicle units rather than the usual multiple hair-follicle units are observed. Results of reciprocal translocation of skin between normal and mutant mice suggest that some diffusible substance synthesized by normal skin can stimulate hair growth and alleviate the hyperkeratosis characteristic of the mutant skin. Homozygotes are viable and fertile, but fertility of females is somewhat reduced ( Gates and Karasek, 1965). See also MGI.

ac, absent corpus callosum, recessive, linkage not known. Discovered accidentally in the course of studies of the brain anatomy of mice with rodless retina ( King and Keeler, 1932). The corpus callosum is partially or completely absent, but a tract of fibers, the longitudinal callosal bundle, which does not occur in normal mice, is present ( King, 1936). A condition similar to that in ac/ac mice and probably genetically identical to it occurs in the BALB/cJ and 129/J strains (Wimer, 1965, personal communication). See also MGI.

ad, adipose, recessive, linkage not known, Chapter 19, 29. Arose spontaneously in a strain selected for large size. Homozygotes are recognizably large than normal between 4 and 5 weeks of age. They may be nearly twice as heavy as normals when adult. Both sexes are probably sterile ( Falconer and Isaacson, 1959; Batt and Harrison, 1963). See also MGI.

ag, agitans, recessive, III. Arose spontaneously in a moderately inbred stock. Homozygotes can be recognized from about 10 days onward. They show retarded growth, generalized tremor, and ataxia. They usually die at weaning but may live as long as 3 months. Atrophy of the Purkinje cells has been found in some regions of the cerebellum ( Hoecker et al., 1954; Martinez and Sirlin, 1955). See also MGI.

Al, alopecia, dominant, VII. Appeared as a spontaneous mutation in the first generation of an outcross. Hair loss is first noticeable at 25 to 30 days. Al/Al mice lose all hair over the body with the exception of some guard hairs. Al/+ mice have more hair but the distinction between Al/Al and Al/+ is not always clear. After the first moult, hair grows in but is lost again at the next moult. Mice appear more patchy as they grow older ( Dickie, 1955). See also MGI.

ald, adrenocortical lipid depletion, recessive, linkage not known. Found in the AKR/O inbred strain by Arnesen ( 1955, 1956). In homozygotes, spontaneous lipid depletion in the adrenal cortex takes place at the time of puberty and depends on the presences of the gonads in both males and females. In adult males the lipid depletion measured as sudanophilia is almost total. In females the depletion is subtotal and shows considerable variation ( Arnesen, 1963). See also MGI.

am, amputated, recessive, linkage not known. Found among the fetuses of dissected pregnant females in an irradiation experiment. Homozygous fetuses lack a tail and at late stages of gestation the limbs appear to have been severed close to the trunk. The head is short and the body edematous dorsally. Vertebrae in the lumbo-sacro-caudal region are absent and these is disorganization of the remainder of the spinal column and some rib fusion. In the forelimbs most of the bones are present but abnormal ( Meredith, 1964). See also MGI.

Amy-1 locus, salivary amylase, linkage group not known, but closely linked to Amy-2. Two codominant alleles are known. Amy-1^a is recognized by a slowly migrating component demonstrated with agar-gel electrophoresis. This allele occurs in several laboratory strains including the C3H, DBA, and AKA. Amy-1^b is recognized by a fast migrating component. Found in a single mouse obtained from a fancier. Amy-1^a/Amy-1^b mice have both bands ( Sick and Nielsen, 1964). See also MGI.

Amy-2 locus, pancreatic amylase, linkage group not known, but closely linked to Amy-1. Two codominant alleles are known. Amy-2^a is recognized by a single band demonstrated with starch-gel electrophoresis. This band migrates faster than either of the bands produced by the Amy-1 locus. Amy-2^b is recognized by two bands of equal strength, one in the same position as that produced by the allele Amy-2^a and another faster migrating band. Amy-2^a/Amy-2^b has 2 bands but the fast one is weaker than the slow one ( Sick and Nielsen, 1964). See also MGI.

an, anemia, recessive, VIII, Chapters 17, 29. X-ray-induced. Homozygotes are anemic at birth, although there is enough variation in the severity of the condition to make classification a little uncertain. Affected mice are small and usually die young. Survivors are sterile ( Hertwig, 1942). The anemia is the normochromic macrocytic type. It can be seen as early as 14 days of gestation and is caused by a disturbance of development of all erythropoietic cells ( Thomas, 1952; Kunze, 1954). The sterility is a secondary effect of the anemia ( Menner, 1957). See also MGI.

ap, alopecia periodica, recessive, linkage not known. Arose spontaneously in an inbred stock at the National Institute of Genetics, Japan. Homozygotes are recognizable at 3 to 4 days of age by their short whiskers and short, sparse first coat. The first coat is shed almost completely between 13 to 15 days and 20 to 24 days. Thereafter the hair is lost and regenerated in cycles which begin at the anterior end and spread toward the tail. During growth of the first coat the skin may have thick scales, and parts of the tail may be lost. All four kinds of hair are present but they are somewhat abnormal ( Tutikawa, 1953). This mutant is not allelic with furless ( fs) nor linked to it ( Tutikawa, 1955). See also MGI.

As, agouti-suppressor, semidominant, V. Found among the offspring of an irradiated (C3H x 101)F₁ male. Very closely inked to the a locus. As appears to suppress the yellow pigment on the middorsum and belly of agouti mice. Homozygotes are darker than heterozygotes with black hair in the ears ( Philips, 1963a). See also MGI.

av, Ames waltzer, recessive, IV. Arose as a mutation in the K strain ( Schaible, 1956). Viability and fertility are about normal, but females are poor mothers. Homozygotes show the typical circling, head-tossing, deafness and hyperactivity of the circling mutants. They have defects of the membranous labyrinth similar to those of sh-2 (Deol, 1965, personal communication). See also MGI.

ax, ataxia, recessive, XV. Arose as a spontaneous mutation in the CBA/H strain. Viability is low; both sexes are sterile. A mutation at the same locus (at first called "paralytic") occurred independently at The Jackson Laboratory. Homozygotes are hyperactive during the second week of life. From the third week on they show a steadily increasing paralysis up to 3 months of age. The paralysis is characterized by tremor, and loss of coordination and weakness of limbs ( Lyon 1955b). In the central nervous system there is degeneration, gliosis, and focal destruction of lower-spinal white matter. The corpus callosum, hippocampal and anterior commissures, and some brain-cell tracts are small ( Coggeshall et al., 1961). See also MGI.

b locus, VIII, Chapter 21. See also MGI.

b, brown, recessive. An old mutant of the mouse fancy. The eumelanin of the hair is brown, rather than black. The pigment granules also appear brown rather than black and are spheroid rather than ovoid in shape ( Markert and Silvers, 1956). Mutations from + to b have been recorded frequently. See also MGI.

B^lt, light, semidominant. Arose as a spontaneous mutation in the C58 inbred strain ( MacDowell, 1950). B^lt/B^lt mice have almost white hair except for the tips which are brown. The pigment granules are the same shape as in b/ b, but somewhat darker in color ( Markert and Silvers, 1956). The granules are clumped ( Quevedo and Chase, 1958; Pierro, 1963a). B^lt/+ mice have darker hair tips and the pigment extends much further down. See also MGI.

b^c, cordovan. Arose as a spontaneous mutation in an F₁ hybrid between C57BL and DBA/1. Recessive to + and dominant to b. The hair color is a rich deep brown ( Miller and Potas, 1955). See also MGI.

ba, bare, recessive, linkage not known. Arose in a strain of Swiss albino mice in 1953 at the Poona Virus Research Centre ( Randelia and Sanghvi, 1951). Homozygotes have no vibrissae at birth. The first coat is much delayed in appearance (13 to 14 days) and the hairs are very thin and short. It is shed at about 30 days. A new hair cycle starts at 45 days but the hairs are thin and are soon shed. Affected mice are entirely naked at 6 months. The number of hair follicles is not reduced, but the follicles contain keratinized globular masses instead of straight hair. The hairs formed are very thin, with no regular internal structure. See also MGI.

bf, buff, recessive, XVII. Arose spontaneously in the C57BL/6J strain. Nonagouti buff mice ( a/ a bf/bf) are khaki colored. Eye color does not appear to be affected ( Dickie, 1964b). See also MGI.

bg, beige, recessive, XIV. Probably radiation-induced. The eye color is light at birth and varies from ruby to almost black in adults. Ear and tail pigmentation is reduced and the coat color is lighter, particularly at the base of the hairs ( Kelly, 1957). There have been at least two recurrences of this mutation or a similar allele. One of them, called slate ( slt) before its allelism with bg was discovered (Lyon, 1965, personal communication), has been described by Pierro and Chase ( 1963, 1965) and Pierro ( 1963b). The pigment granules are reduced in number but larger in size in the cortex and medulla of the hair and in the melanocytes of the choroid and retina of the eye and of the Harderian gland. The granules are clumped in the medulla of the hair. The smaller number of granules is due both to the synthesis of fewer melanin granules and to the fusion of individual granules into progressively larger clumps. Temporary hair loss during the third week of life occurs in some homozygotes. See also MGI.

bh, brain-hernia, recessive, probably I, Chapter 29. Appeared as a spontaneous mutation in the second generation following an outcross. Viability of homozygotes is reduced but some survive and may breed well. Penetrance is probably variable and dependent on the genetic background. At birth homozygotes may have cerebral hernia, hydrocephaly, anophthalmia, or microphthalmia. Later in life they all develop polycystic kidneys ( Bennett, 1959). The polycystic disease is preceded by the appearance of PAS-positive plugs in the tubules of the kidney. Analysis of the urine shows that bh/bh mice have a higher than normal level of free amino acids and protein prior to the development of the disease ( Bennett, 1961a). See also MGI.

Bld, blind, semidominant, linkage not known. Arose spontaneously in the Bagg albino strain. Heterozygotes are born with their eyelids open and the cornea becomes damaged. Homozygotes die at the end of the seventh day of gestation. Primitive streak and mesoderm fail to form. Entoderm appears very abnormal. In the proximal entoderm the cells are greatly enlarged and may be polyploid. The over-all size of the egg cylinder is about one-fifth that of the normal ( Vankin, 1956). Penetrance in the heterozygote is incomplete ( Watson et al., 1961). The mutation recurred at Harwell, England ( Watson, 1962). See also MGI.

Blo, blotchy, semidominant, XX (sex-linked), Chapter 15. Arose spontaneously. Heterozygous females have irregular patches of light-colored fur. Expression is occasionally poor at weaning age but is complete at adulthood. Hemizygous males and homozygous females are light all over with no blotching, are usually small, and occasionally have deformed hind legs. Viability and fertility of heterozygotes is normal. Hemizygotes and homozygotes have reduced viability and many are infertile ( L.B. Russell, 1960b). Blo may be an allele of Mo. See also MGI.

Bn, bent-tail, semidominant, XX (sex-linked), Figure 8-2A, Chapter 15. Appeared as a spontaneous mutation in a crossbred male. Tails of heterozygous females are more or less shortened, with one or several bends. Penetrance is incomplete. Tails of homozygous females and hemizygous males are shorter and more kinked and not always clearly distinguishable from the tails of heterozygotes. Heterozygous females have normal viability and fertility, but homozygotes and hemizygotes may be less viable and fertile than normal ( Garber, 1952b, Grüneberg, 1955b). See also MGI.

bp, brachypodism, recessive, V, Chapter 15. Arose in a stock of Swiss mice at Harvard University. Fully viable and fertile. The phalangeal bones of all four feet are reduced in number, the metacarpals and metatarsals are shortened and all other bones of the feet are small and irregular in shape. The long bones of the legs are significantly shortened ( Landauer, 1952). There have been at least two recurrences of this mutation or a similar allele. See also MGI.

Bph, brachyphalangy, semidominant, linkage not known. Found in a low-intensity neutron irradiation experiment. In heterozygotes, digits of the forefeet are splayed out with marked shortening and thickening of phalanges and metacarpals. Hind feet are less severely affected. Homozygotes die before birth, all feet showing brachyphalangy and high grade polydactyly. There are other severe limb defects and frequently exencephaly ( Searle, 1965). See also MGI.

bt, belted, recessive, VI, Chapter 21. Arose as a spontaneous mutation in the DBA inbred strain ( Murray and Snell, 1945). Homozygotes have a white belt across the back in the midtrunk region and a white belly patch. The two may coalesce to form a complete belt. The white spotting appears to be due to a defect in the hair follicles which prevents pigment cells either from entering the hair follicles or from developing there ( Mayer and Maltby, 1964). See also MGI.

c locus, I, Chapter 21. The albino locus affects the amount of tyrosinase in the pigment cells, but does not interfere with the production of pigment cells themselves ( Coleman, 1962; Silvers, 1958). It is probably the structural locus for tyrosinase. All the mutant alleles are recessive to wild type in appearance, but heterozygotes with wild type produce intermediate amounts of tyrosinase. Spontaneous mutation at this locus appears to be relatively infrequent. See also MGI.

c^ch, chinchilla. First described by Feldman ( 1922). Agouti chinchilla mice are gray rather than brownish gray. The yellow pigment in the hair is greatly reduced and the black pigment slightly so. Eyes are black. Tyrosinase activity in the skin is about one-third that of normal ( Coleman, 1962). Heterozygotes with c^h, c^e, and c are intermediate both in color and in tyrosinase activity. See also MGI.

c^e, extreme dilution. Found in the wild by Detlefsen ( 1921). Hair is very light gray and eyes are black. Tyrosinase activity in the skin is very low ( Coleman, 1962). c^e/ c are almost white with black eyes. See also MGI.

c^h, himalayan. Found in the offspring of a cross between the DBA/2 and AKR/J strains. Body hair is light and ears, nose, and tail are dark as in Siamese cats. Body hair may be very light or quite sooty, depending on the genetic background. Eyes are slightly pigmented and appear red. c^h/ c and c^h/ c^e are intermediate between the homozygotes ( Green, 1961a). The tyrosinase of c^h/c^h mice is temperature sensitive ( Coleman, 1962). See also MGI.

c, albino. A very old mutant, already known in Greek and Roman times. Hair and eyes are completely devoid of pigment. Tyrosinase activity is almost absent ( Coleman, 1962). See also MGI.

Ca, caracul, dominant, VI. Arose in a stock of Swiss mice ( Dunn, 1937b). Homozygotes are indistinguishable from heterozygotes. Both are fully viable and fertile. Vibrissae are curved and hair is wavy from time of first appearance until about 4 weeks of age. After that the waves disappear but the hair has a plush-like look. Several recurrences of mutations at this locus similar to Ca have been reported. See also MGI.

Cat, dominant cataract, dominant, linkage not known, Chapter 29. Arose in an albino strain of unknown origin ( Paget, 1953). Homozygotes and heterozygotes are fully viable and fertile. They are indistinguishable except that the age of onset may be earlier in homozygotes. Age of onset varies between 10 days and 14 weeks. Liquefaction of the subcapsular zone of the lens leads to cataract of the cortex and the lens nucleus. The lens capsule always remains intact. With the exception of the nucleus the whole lens material may become liquified and much of it may pass through the intact lens capsule into the vitreous ( Paget and Baumgartner-Gamauf, 1961). An allelic mutant, originally called shrivelled ( Svl) was found in the A/J strain by Fraser and Schabtach ( 1962) ( Verrusio, 1964). See also MGI.

cb, cerebral degeneration, recessive, linkage not known. Found by Deol and Truslove ( 1963). Homozygotes usually die before reaching maturity. If they live on they are always sterile. The degeneration produces an ex vacuo hydrocephalus visible in the living animal and usually recognizable at birth. The most susceptible parts of the brain are the cerebral hemispheres and olfactory lobes. Later the epithelium of the nose and trachea also degenerates. See also MGI.

Cd, crooked, semidominant, linkage not known. Arose spontaneously in the A inbred strain ( Morgan, 1954). Heterozygotes have crooked tails with abnormal caudal vertebrae and often have abnormal sacral and lumbar vertebrae as well. Some have no abnormalities of the skeleton at all. Homozygotes are more severely affected and show no normal overlapping. They may die early in development, or later with exencephaly, or, if they survive, are much smaller than normal from about fifteen days of age and may have crooked tails, microphthalmia, small or nonerupted lower incisors, absence of third molars, irregular tail rings with few hairs, and nervous movement of the head ( Morgan, 1954; Grewal, 1962a). The vertebral anomalies can be traced back to the somite stage when the somites are seen to be irregular in size and often partly fused with their neighbors ( Matter, 1957). See also MGI.

Ce, low liver catalase, dominant, linkage not known, Chapter 19. This mutant reduces liver catalase activity to about half its normal level but has no effect on kidney catalase. The low allele is fully dominant over the normal allele. The low allele is found in most of the C57 family of strains including C57BL/6, C57BL/10, C57L, C57BR/cd, and C58/Lw, but not in C57BL/He and C57BL/An. The normal allele occurs in C3H/He, YBR/He, and BALB/cDe ( Rechcigl and Heston, 1963; Heston and Rechcigl, 1964; Heston et al., 1965). See also MGI.

ch, congenital hydrocephalus, recessive, XIV. Appeared as a spontaneous mutation in descendants of an outcross of the CBA inbred strain ( Grüneberg, 1943a). Homozygotes die immediately after birth, possibly from inability to inflate their lungs. They are very uniform in appearance, with bulging forehead, and with twin protuberances corresponding to the cerebral hemispheres and filled with hemorrhagic fluid. Development of cartilage is severely affected, beginning at the mesenchymal stage. The mesenchymal condensations are smaller than normal, the reduction being more marked in some parts than in others. Once laid down, cartilages grow at a normal rate but may be abnormal in shape. May are absent altogether. The hydrocephalus is due to an abnormal shortening of the base of the skull ( Grüneberg, 1953b). See also MGI.

cl, clubfoot, recessive, linkage not known. Appeared in a stock of unknown ancestry. Homozygotes are much less viable and fertile than normal. The clubbing is a simple calcaneum (dorsiflexed) type, always affecting both hind feet and sometimes one or both forefeet. Muscles of the lower limb are smaller than normal and there is some carpal and tarsal fusion ( Robins, 1959). See also MGI.

cn, achondroplasia, recessive, linkage not known, Figure 8-1H, Chapter 29. Arose in strain AKR/J in 1960. Homozygotes show a disproportionate dwarfing which is probably due to abnormal growth of the epiphyses. Viability is considerably reduced and very few of the survivors are fertile ( Dickie, 1961). See also MGI.

cr, crinkled, recessive, XIV. Appeared in the progeny of a male treated with nitrogen mustard. Homozygotes are characterized by absence of guard hairs and zigzag hairs in the coat. This produces a bald patch behind the ears, and a bald tail, and also leads to kinks at the tail tip, reduced aperture of the eyelids, respiratory disorder, and a modification of the agouti pattern. The hair follicles that produce guard hairs and zigzags develop at 14 to 17 days of gestation and after birth, respectively. These follicles are absent in cr/cr. The viability and breeding performance of homozygotes is somewhat reduced ( Falconer et al., 1951). See also MGI.

ct, curly-tail, recessive, linkage not known. Arose spontaneously in the GFF inbred strain. Genetic data indicate that ct is probably a recessive with incomplete penetrance (20 to 50 per cent) but do not absolutely rule out the possibility that it is a dominant with reduced penetrance. Presumed homozygotes, if abnormal, usually have some degree of spina bifida and, occasionally, anencephaly. If the mice survive, the spina bifida usually results in a curly of kinky tail ( Grüneberg, 1954a). See also MGI.

cv, calvino, recessive, linkage not known. Arose in the C58/Hr inbred strain. The first coat of homozygotes is somewhat sparse. Adults have a reduced quantity of all hairs, especially zigzags. Males are more affected than females, and the back is more affected than the belly. There is extensive silvering of the hair. Calvinos are usually underweight and often sterile ( Pizarro, 1957).

cw, curly whiskers, recessive, II. Arose in the CBA strain maintained at the Chester Beatty Research Institute, London. Homozygotes have strongly curled whiskers; their coats are not waved but slightly abnormal in appearance. Heterozygotes have slightly bent whiskers but cannot be reliably identified on this basis ( Falconer and Isaacson, 1962b). See also MGI.

d locus, II, Chapters 21, 23, 32. Mutations at this locus alter coat color, reduce phenylalanine hydroxylase activity ( Coleman, 1960), and affect the nervous system. Mutations from + to d^l and from d to + have been observed repeatedly. See also MGI.

d, dilute, recessive. An old mutant of the mouse fancy. The blue-gray color of the hair produced by this mutant in nonagouti ( a/ a) mice is caused by clumping of the melanin pigment into a few large masses ( E.S. Russell, 1949a). The clumping is due to the shape of the melanocytes which have fewer and thinner dendritic processes than wild-type melanocytes, with the result that melanin granules are largely clumped around the nucleus ( Markert and Silvers, 1959). See also MGI.

d^l, dilute-lethal, recessive to both + and d. Arose in the C57BL/Gr inbred strain. The color of d^l/d^l is identical to that of d/ d, but the mice develop a severe neuromuscular disorder characterized by convulsions and opisthotonus (arching upward of the head and tail) and usually die at about 3 weeks ( Searle, 1952). Myelin degeneration occurs in the central nervous system ( Kelton and Rauch, 1962). Phenylalanine metabolism is severely disturbed ( Rauch and Yost, 1963). See also MGI.

d^s, slight dilution, recessive. Discovered in a C57BL/6J x DBA/2 hybrid. Homozygotes are darker than d/ d mice. d^s/ d is intermediate between d^s/d^s and d/ d. See also MGI.

d¹⁵, dilute-15, recessive to +. Homozygotes have slightly diluted coats, darker than d/ d. They develop behavioral abnormalities similar to d^l/ d^l at about 20 days but some may live, one male surviving to breed. d/d¹⁵ are similar in color to d¹⁵/d¹⁵ but behave normally ( Phillips, 1962). See also MGI.

da, dark, recessive, I. Arose in the CBA/Fa inbred strain. Probably extinct. Homozygotes are smaller than normal. In combination with A or A^y the yellow pigment on the back is replaced by black so that both look like a/ a except on the flanks. The darkening of the back of A lessens as the animals get older ( Falconer, 1956). See also MGI.

Dc, dancer, semidominant, linkage not known. Arose as a spontaneous mutation in the C3H/J- ob stock ( Lane, 1958). Not allelic with Tw, which it somewhat resembles. Viability and fertility of heterozygotes are normal. Penetrance is incomplete in heterozygotes. Homozygotes die at birth with cleft lip and cleft palate. Heterozygotes exhibit circling and head-tossing behavior, but are not deaf. They usually have a small patch of white hairs on the forehead. There is complete absence of the macula of the utriculus accompanied by gross defects of the bony and membranous labyrinths in the vestibular region (Deol, 1965, personal communication). See also MGI.

de, droopy-ear, recessive, XVI. Arose spontaneously in the J stock at the Institute of Animal Genetics, Edinburgh. In homozygotes the ears are set low on the sides of the head and the pinnae project laterally. On an a^t background the light belly hair comes farther around the sides of the body and face. Homozygotes tend to be smaller than their sibs but they breed well, except that some females are poor mothers. The skeleton of the occiput and shoulder girdle shows specific abnormalities, while the rest of the skeleton shows immaturity of form with disproportionate shortening of the limb bones. The skeletal abnormalities can be traced back to disturbed mesenchymal condensations. It is possible that the growth of cartilage itself is also abnormal ( Curry, 1959). See also MGI.

df, Ames dwarf, recessive, VIII, Chapters 20, 29. Arose spontaneously in descendants of a cross of Goodale giant mice to a pink-eyed stock. Homozygotes resemble dw/ dw mice. Growth retardation occurs after the first week and weight at 2 months is only about one-half normal. Both sexes are sterile. Treatment with bovine growth hormone for 6 weeks produces nearly normal growth and males become fertile ( Schaible and Gowen, 1961). The anterior hypophysis lacks acidophils and has very few thyrotropic hormone-producing cells ( Bartke, 1964). See also MGI.

Dh, dominant hemimelia, semidominant, XIII, Chapter 15. Arose spontaneously in a crossbred stock. Heterozygotes show preaxial polydactyly or oligodactyly of the hind limbs, tibial hemimelia, and sometimes reduction of the femur and pubic element of the pelvic girdle. Number of ribs, sternebrae, and presacral vertebrae tend to be reduced. The spleen is entirely lacking; the stomach is somewhat smaller and the alimentary canal shorter than normal. Homozygotes die within a few days after birth. Abnormalities are similar to those of heterozygotes but much more severe and include also abnormalities of the urogenital system ( Searle, 1964). See also MGI.

di, duplicate incisors, recessive, linkage not known. Found in F₂ generation from mice treated in utero with nitrogen mustard. Penetrance is high in mice of the original stock, but low and variable in descendants of outcrosses. Affected mice are characterized by the appearance on one or both sides of supernumerary lower incisors located directly behind, or slightly medial to the corresponding normal teeth. The extra teeth usually erupt a few days later than the normal incisors. Usually they become deflected and are broken off, after which it may be difficult to say whether an extra tooth had ever been present ( Danforth, 1958). See also MGI.

dl, downless, recessive, probably IV. Appeared in strain A/H. Homozygotes closely resemble homozygous crinkled ( cr) mice, but the two mutants are not allelic. Defects of the incisors prevent the mice from eating hard food ( Phillips, 1960b). See also MGI.

dm, diminutive, recessive, V, Chapters 15, 17. Appeared in descendants of a cross of strains 129 and C57L/J. Viability of homozygotes is low but many surviving to maturity are fertile. Homozygotes are consistently smaller than normal and have a macrocytic anemia which becomes slightly less severe with age. They have short kinked tails and tend to have an additional rib at both the cervical and lumbar ends of the thorax, and an additional presacral vertebra. The vertebrae are malformed and ribs may be fused ( Stevens and Mackerson, 1958). See also MGI.

dn, deafness, recessive, linkage not known, Chapter 32. Discovered in a stock at the University College, London, in the course of a systematic search for uncomplicated deafness ( Deol and Kocher, 1958). Fertility of homozygotes is normal. Homozygotes are deaf their entire life, and few of them show slight head-tossing. Degeneration of the cochlea begins on the 10th day. The macula of the sacculus may degenerate in both head-tossing and normally behaving mice, but remains histologically normal in many of them. See also MGI.

dr, dreher, recessive, XIII, Chapter 32. Arose in the wild, presumably as a spontaneous mutation, and was obtained in a litter of four, all homozygous, captured in a factory in Detmold, Germany ( Falconer and Sierts-Roth, 1951). Homozygotes show the circling, head-tossing, deafness, and hyperactivity characteristic of the circling mutants. They may also have a partial or complete white belt ( Lyon, 1961a). The bony and membranous labyrinths develop abnormally and there may be hydrocephalus of the hindbrain (Fisher, 1956, 1958; Bierwolf, 1956, 1958). The defects of the ear and hindbrain trace back to an abnormality of the neural tube at 9 days of gestation. The roof of the posterior part of the rhombencephalon, normally very thin, in dr/dr embryos is thick like that of the neural tube in the cervical region, as though joining of the lateral plates had extended more anteriorly than normal ( Deol, 1964b). See also MGI.

Ds, disorganization, semidominant, III. Arose spontaneously in the inbred DA/Hu strain. Ds disrupts the orderly process of development. Homozygotes probably die in utero after implantation and before term. Heterozygotes are normal, deviate slightly, or are monstrous individuals with multiple defects. The defects show great variety, range of severity, and random distribution among derivatives of all germ layers. Penetrance varied between 9 and 89 per cent on different genetic backgrounds observed by Hummel ( 1958, 1959). See also MGI.

dt, dystonia musculorum, recessive, XIII, Figure 8-2F. Arose spontaneously in mice bred at the Institute of Animal Genetics, Edinburgh. Homozygotes can be first recognized at 7 and 10 days of age by clasping of the hind limbs when the mice are lifted by the tail. There is increasing incoordination with alternating hyperextension and hyperflexion of the limbs. There is no obvious paralysis. Many affected animals die before weaning, but some survive several months. The clinical condition becomes relatively stationary after the first phase of deterioration. Histologically the nervous system shows widespread degeneration and loss of nerve fibers in the peripheral nerves, dorsal root ganglia, and roots, and in the dorsal and ventrolateral columns of the spinal cord. In longer surviving animals there is also evidence of lower motor neurone involvement ( Duchen and Strich, 1964). There have been several recurrences of mutation at this locus at The Jackson Laboratory. See also MGI.

du, ducky, recessive, II. Arose as a spontaneous mutation in a noninbred stock ( Snell, 1955). Viability is somewhat less than normal. Males living to maturity may be fertile but are poor breeders. Females rarely breed. Homozygotes show a waddling or reeling gait and a tendency to fall to one side. They are slightly smaller than their normal sibs and may occasionally have seizures. See also MGI.

dv, dervish, recessive, linkage not known. Possibly radiation-induced. Homozygotes are viable ( L.B. Russell, 1961). No tests for allelism with other waltzing mutants have been reported. See also MGI.

dw, dwarf, recessive, linkage not known. Arose in a stock of silver mice obtained from an English fancier ( Snell, 1929). Homozygotes are about one-fourth to one-third normal size and are sterile. The small size is due to a defective anterior pituitary in which there is a great deficiency of acidophils and also a deficiency of motor neurone cells ( Elftman and Wegelius, 1959). Dwarf mice grow to normal size and may become fertile when given daily implants of whole pituitaries ( Smith and MacDowell, 1930). See also MGI.

dy, dystrophia muscularis, recessive, IV, Figure 8-1C, Chapters 19, 29. Arose as a spontaneous mutation in the 129/Re inbred strain. Homozygotes are characterized by progressive weakness and paralysis beginning at about 3 ½ weeks of age. The hind limbs are affected first, later the axial and forelimb musculature. Death usually occurs before 6 months of age and the mice are usually sterile. There is no demonstrable pathology of the nervous system, but the muscular tissue shows degeneration typical of the muscular dystrophies, with proliferation of sarcolemmal nuclei, increase in amount of interstitial tissue, and size variation among individual fibers ( Michelson et al., 1955). See also MGI.

Ea-1 locus, erythrocyte antigen-1, linkage not known. Wild population of house mice have been found to contain four phenotypes with respect to erythrocyte antigens, designated A, B, AB, and O and appearing to be under the control of a system of three alleles, Ea-1^a, Ea-1^b, Ea-1^o. The locus appears to differ from the H-2 locus. Erythrocytes of 13 inbred strains lacked both A and B antigens ( Singer et al., 1964). See also MGI.

eb, eye-blebs, recessive, IV. Arose in a noninbred stock of hairless mice. It resembles my but is not allelic to it. Penetrance is incomplete. Homozygotes may be normal or have defects of the eyes, kidney, or feet including: anophthalmia or microphthalmia; small, missing, or cystic kidneys; and clubbed feet, webbed toes, or extra digits ( Hummel and Chapman, 1963). See also MGI.

ec, ectopic, recessive, linkage not known. Found among the descendants of mice exposed to 1,000 R of X-rays. Homozygotes are first distinguishable from normal at 28 to 30 days, when there is a slight increase in the size of the eyeball. The increase disappears after 6 weeks. At 5 weeks an opacity of the lens develops. The nucleus of the lens is gradually displaced through the posterior pole of the ruptured capsule. Histologically the lens epithelium is abnormal at about 4 weeks. In normal mice it is a single layer with no mitotic figures but in ec/ec mice the epithelium is irregularly stratified with many mitotic figures. The posterior part of the lens capsule is much thinner than normal ( Beasley, 1963). ec is similar to lr but allelism tests have not been made. See also MGI.

Ee-1 locus, erythrocytic esterase-1, linkage not known. Independent of Ee-2. Two codominant alleles are known, Ee-1^a and Ee-1^b, which produce esterases with different electrophoretic mobility. Both alternative molecular forms are sensitive to diisopropyl fluorophosphate. Ee-1^a is found in inbred strains C57BL/6, C57BL/10, and C57BR/cd. Ee-1^b is found in strains AT, BALB/c, SEC/Re, A/He, C3H/He, CBA/J, and DBA/2J ( Pelzer, 1965). See also MGI.

Ee-2 locus, erythrocytic esterase-2, linkage not known. Independent of Ee-1. Two alleles at this locus control the presence (Ee-2^a) or absence (Ee-2^o) or an erythrocytic esterase inhibited by eserine. Ee-2^a is found in strains A/He, C3H/He, CBA/J, and DBA/2J. Ee-2^o is found in strains C57BL/6, C57BL/10, C57BR/cd, AT, BALB/c, and SEC/Re ( Pelzer, 1965). See also MGI.

Eo, eye-opacity, dominant, linkage not known. Radiation-induced. Eye-opacity and small eyes, and occasionally open lids at birth ( Gower, 1953). See also MGI.

ep, pale-ears, recessive, XII. Arose as a spontaneous mutation in the C3HeB/FeJ inbred strain. The ears and tail are pale in color. The juvenile coat is slightly diluted in color but the adult coat is almost normal. Eyes are pale at birth and darken with age. ep is an almost exact mimic of le but not allelic to it (Lane and E.L. Green, 1965, personal communication). See also MGI.

Er, repeated epilation, dominant, linkage not known. Probably radiation-induced. Homozygotes probably die prenatally. There is complete penetrance in heterozygotes. They grow a normal appearing but probably somewhat dry coat until the age of about 13 days; then hair loss begins until the fur becomes sparse. Repeated growth and re-epilation follow without any definite pattern. Heterozygotes are slightly reduced in size bur completely viable and fertile ( Hunsicker, 1960). See also MGI.

Es-1 locus, serum esterase-1, XVIII, Chapter 15. This locus controls a difference in electrophoretic mobility on starch gel of a serum esterase which has a mobility similar to that of serum albumin. Two codominant alleles are known: Es-1^a, which produces a faster migrating single band and is present in C57BL/Cum and C57L/Rl; and Es-1^b, which produces a slower double band and is present in many other inbred strains ( Popp and Popp, 1962; Popp, 1965a). See also MGI.

Es-2 locus, serum esterase-2, linkage not known, Chapter 15. This locus controls variation in the fastest anodally migrating serum esterase as revealed by starch-gel electrophoresis at pH 8.5. Two alleles are known: Es-2^a, absence of the esterase band, found in a wild mouse from Washtenaw County, Michigan; and Es-2^b, presence of the esterase band, present in many inbred laboratory strains. Es-2^a/Es-2^b produces a lighter band than Es-2^b/Es-2^b ( Petras, 1963). See also MGI.

Es-3 locus, kidney esterase-3, linkage not known. Independent of Es-4. This locus controls variation in a kidney esterase revealed by vertical starch-gel electrophoresis at pH 8.65. Two allele are known: Es-3^a, absence of the esterase band, found in inbred strain C57BL/6J; and Es-3^b, presence of the esterase band, found in inbred strain RF/J. Es-3^a/Es-3^b is recognizable by a lighter band than in Es-3^b/Es-3^b. There are five zones of banding of kidney esterases, and this esterase is found in the fastest migrating region of zone IV, numbered from the origin. The esterase is sensitive to inhibition by eserine sulfate ( Ruddle and Roderick, 1965). See also MGI.

Es-4 locus, kidney esterase-4, linkage not known. Independent of Es-3. This locus controls variation in a kidney esterase revealed by vertical starch-gel electrophoresis at pH 8.65. Two alleles are known: Es-4^a, absence of the esterase band, found in inbred strain C57BL/6J; and Es-4^b, presence of the esterase band, found in inbred strain RF/J. Es-4^b is dominant to Es-4^a. The esterase band occurs in the cathodal region of zone IV (see Es-3) ( Ruddle and Roderick, 1965). See also MGI.

et, elevated-tail, recessive, linkage not known. Arose spontaneously in the BALB/c inbred strain. In homozygotes the tail emerges high and is about two-thirds normal length and wavy ( L.B. Russell, 1951).

ey-1, eyeless-1, ey-2, eyeless-2, linkage not known. Chase ( 1942, 1944) postulated that microphthalmia and anophthalmia observed in nearly 90 per cent of the mice in certain selected strains. It is not certain that two discrete loci with large effects exist (Beck, 1963a, b). If they exist they are not yet distinguishable from each other either by their effects or by known linkage map position. Mice heterozygous at one or both of these loci have a higher incidence of abnormal eyes than homozygous normal mice as a result of trypan blue injected into their mothers during gestation ( Barber, 1957; Beck, 1963c). See also MGI.

f, flexed-tail, recessive, XIV, Chapters 17, 21. Homozygotes are born with a transitory siderocytic anemia caused by disturbance of the hematopoietic function of the fetal liver. Most homozygotes also have flexed tails and a belly spot, but these are not constant manifestations of the mutant. Because of the anemia there is probably slightly greater postnatal mortality among f/f than among normal mice. The anemia begins on the 12th day of embryonic life when the liver first starts to produce blood cells ( Grüneberg, 1942a). Both heterozygotes and homozygotes have low levels of liver δ-aminolevulinate dehydratase ( Margolis, 1956). Flexed is closely linked to Lv and may be an allele (Coleman and E.S. Russell, 1965, personal communication). The tail abnormalities are first noticeable on the 14th day as abnormal differentiation of the fibers of the annulus fibrosis of the intervertebral discs. Kinking of the tail results, as well as occasional fusions of the other vertebrae ( Kamenoff, 1935). See also MGI.

fa, falter, recessive, linkage not known. Arose as a spontaneous mutation in a DBA subline. Homozygotes have an abnormal side-to-side swaying walk beginning at about 10 days of age. The abnormality becomes more pronounced with age and all mice die at about 20 days. fa has not been tested for allelism with other similar mutants ( Yosida, 1960). See also MGI.

fi, fidget, recessive, V, Chapters 15, 32. Discovered by Grüneberg ( 1943b) in a heterozygous strain. Viability of homozygous fidgets is usually less than normal and may be as low as 50 per cent on some genetic backgrounds. Fertility is poor but some males are reliable breeders. Homozygotes toss their heads from side to side and tend to run in circles but can hear throughout life. The bony labyrinth is quite defective. There are other abnormalities including small eyes, absence of lachrymal glands, dislocation of the hip, increased incidence of polydactylism, and displaced parafloccular lobes of the cerebellum ( Truslove, 1956). See also MGI.

fl, flipper-arm, recessive, linkage not known. Probably radiation-induced. Viability of homozygotes is poor. Males are sterile, females only occasionally fertile. Homozygotes are smaller than their normal sis. The ulna and radius bend sharply outward near the wrist. The hind limbs are normal ( Kelly, 1957). See also MGI.

fm, foam-cell reticulosis, recessive, linkage not known. Arose spontaneously in the CBA/H strain. In homozygotes lipid-containing foam-cells replace the lymphoid tissue of the thymus and Peyer's patches and occur in smaller numbers in other tissues. The lipid may be a complex of lysolecithin and cholesterol and the disease is similar to Nieman-Pick disease in man. It is first detectable in mice 3 to 4 months old, and death occurs within a few weeks ( Lyon et al., 1965). See also MGI.

fr, frizzy, recessive, I. Arose in a stock of mixed origin at The Jackson Laboratory. Homozygotes have wavy or curly vibrissae at 1 or 2 days after birth. The coat is short and rough at first and then may become normal at 6 or 7 weeks. It is usually short and thin in older animals ( Falconer and Snell, 1952). Following some outcrosses the proportion of fr/fr mice identifiable in the F₂ is low, an indication that penetrance may be low on some backgrounds. See also MGI.

fs, furless, recessive, XIV. Appeared in an unpedigreed stock maintained in the Department of Zoology at Ohio State University. Homozygotes have short or missing vibrissae 2 days after birth. The first coat grows normally but begins to thin out at 19 days, starting on the head. A new coat grows but persists only a short time. Mature mice are partly devoid of hair at all times. The hairs present are shorter than normal. Furless mice are slightly smaller than their normal sibs but are normally fertile ( Green, 1954). See also MGI.

ft, flaky tail, recessive, linkage not known. Discovered in a heterozygous stock. Homozygotes have flaky tails, often with constrictions resulting in amputation of the tail, and slightly smaller than normal ears. The stratum granulosum is thinner than normal, presumably resulting in slower than normal proliferation of the stratum corneum and keratin ( Lane and Green, 1962). See also MGI.

Fu locus, IX. See also MGI.

Fu, fused, semidominant. Arose in stocks at the Bussey Institution prior to 1931. Expression of this mutant shows greater variability. Both homozygotes and heterozygotes may have shortened and kinked tails or they may both be normal. Homozygotes tend to be more severely affected than heterozygotes. Expression is not dependent on the residual genotype but offspring of Fu/+ or Fu/Fu mothers are less likely to express the character than offspring of +/+ mothers ( Reed, 1937). Homozygotes and heterozygotes occasionally show an abnormal behavior similar to the circling mutants and are deaf ( Dunn and Caspari, 1945). Embryos of homozygotes show some overgrowth and duplication of the posterior part of the neural tube ( Theiler and Gluecksohn-Waelsch, 1956). See also MGI.

Fu^ki, kinky, semidominant. Arose in the stocks of a Florida mouse fancier ( Caspari and David, 1940). Heterozygotes are very similar to fused in abnormalities of the skeleton and may show the same behavioral abnormalities. Dunn and Caspari ( 1945) found five probable crossovers between Fu and Fu^ki among 505 gametes tested, but Dunn and Gluecksohn-Waelsch ( 1954) found none in 971 and concluded that the previous study was in error and that kinky is an allele of Fu. Unlike Fu, kinky homozygotes are inviable. They show tissue hyperplasia and twinning at 7 days and die between 8 and 10 days of embryonic life ( Gluecksohn-Schoenheimer, 1949). See also MGI.

fy, frowzy, recessive, linkage not known. Arose spontaneously in either the C3H or 101 inbred strain. Homozygotes are viable and usually fertile. The skin is wrinkled and the hair is sparse and frizzy. Vibrissae are curly. Ear tufts are absent, and feet, nose and tail are white ( Major and Hawkins, 1958, as "hair abnormality"). See also MGI.

fz, fuzzy, recessive, XIII. Discovered in 1945 in the CFW stock at Carworth Farms. Homozygotes are viable and fertile. They are classifiable at 6 days of age by their thin, wavy vibrissae and uneven coat. In the adult the coat is thin and wavy or curly. Penetrance seems to be complete ( Dickie and Woolley, 1950). Follicles of all hair types are present in the skin of newborn mice, but the structure of the hair is altered ( Mann, 1964). See also MGI.

g, low glucuronidase, recessive, XVII, Chapter 19. Several sublines of the C3H strain (C3H/He, C3H/Ha) produce a low level of liver β-glucuronidase. The low level behaves as if controlled by a single recessive gene in crosses with strains having normal levels (CBA/St, CBA/An, C57BL. BALB/c, DBA/2, RIII) ( Law et al., 1952). In g/g mice the intracellular distribution of the enzyme as well as the time course of accumulation in the liver is different from that of +/- mice. The enzyme of g/g mice differs in susceptibility to heat denaturation and to inactivation by alkali from that of +/+ mice and is therefore presumably different in structure (Paigen, 1961a, 1961b, 1964). See also MGI.

gl, grey-lethal, recessive, IV, Chapters 15, 20, 29. Arose spontaneously in a stock segregating for c^e ( Grüneberg, 1935b). Homozygotes die between 20 and 30 days of age. Most of the yellow pigment is absent from the fur, resulting in a slate gray color in agouti mice. The color of a/ a mice is not noticeably influenced by gl. Homozygotes lack the power of secondary bone resorption. Consequently the bones cannot grow normally, they do not form normal marrow cavities, and the teeth do not erupt. An atlas of the skeletal anatomy of grey-lethal and normal sibs at 3 weeks of age has been prepared by Bateman ( 1954). Grey-lethals are considerably more resistant to injections of parathyroid hormone than normal mice (Barnicot, 1945, 1948). Evidence favors the hypothesis that failure of secondary bone resorption is due to an accelerated rate of inactivation of parathormone ( Hirsch, 1962). See also MGI.

gm, gunmetal, recessive, linkage not known. Arose spontaneously in the C57BL/6J inbred strain. Homozygotes have a diluted coat color somewhat similar to that of dilute ( d/ d). Eye color does not appear to be affected. Homozygotes have high mortality and do not breed well ( Dickie, 1964b). See also MGI.

go, angora, recessive, probably XVII. Arose spontaneously in the BALB/cJ inbred strain. Homozygotes are recognizable at about 18 days by the extra length of the guard hairs. At weaning the guard hairs are more than twice normal length. Vibrissae are also very long ( Dickie, 1963). See also MGI.

gp, gaping lids, recessive, linkage not known. Not allelic with oe or lg ( Miller, 1964) but has not been tested for allelism with lo. Arose in a stock carrying ax. In homozygotes the eyes are open at birth, and become opaque with age. Homozygotes are viable and fertile. The gene appears to have full penetrance. From 15 days of gestation onward the lens is about twice normal size ( Kelton and Smith, 1964). See also MGI.

gr, grizzled, recessive, X. Homozygotes resemble c^ch/ c^ch mice. The yellow pigment becomes white, but the black pigment is unaffected. In combination with nonagouti the hair on the ears and genitalia is white instead of yellow ( Falconer, 1950). Segregation is abnormal with a deficiency of gr/gr which is due to prenatal mortality from unknown causes ( Bloom, 1962). See also MGI.

Gs, greasy, semidominant, XX (sex-linked). Discovered among later descendants of an irradiated male but is probably of spontaneous origin. Possibly an allele of Ta. Gs/+ resembles Ta/+. Homozygous females and hemizygous males have shiny fur like the corresponding Ta genotypes but lack the bare patches behind the ears, the dark middorsal stripe in agouti mice, and the characteristic sticky feel of the tail ( Larsen, 1964). See also MGI.

Gy, gyro, semidominant, XX (sex-linked). Hemizygous males show circling behavior, abnormal development of the long bones and ribs, and are sterile. Heterozygous females show incomplete penetrance of the circling behavior and no bony abnormalities have been detected ( Lyon, 1961b). See also MGI.

H-1 locus, histocompatibility-1, I. For this and other histocompatibility loci see Chapter 24. See also MGI.

H-2 locus, histocompatibility-2, IX. See also MGI.

H-3 locus, histocompatibility-3, V. See also MGI.

H-4 locus, histocompatibility-4, I. See also MGI.

ha, hemolytic anemia, recessive, linkage not known, Chapter 17. Arose spontaneously in the DBA/1J inbred strain. Homozygotes show neonatal hypochromic anemia, microcytosis, and jaundice. The abnormality is not the result of either maternal-fetal incompatibility or the presence of abnormal hemoglobin. Many die within a few days after birth but occasional animals survive 6 months or more. All are sterile ( Bernstein, 1963). See also MGI.

Hba locus, hemoglobin α-chain, linkage not known, Chapter 17. The several alleles at this locus were first recognized by their effect on the solubility of carbon monoxyhemoglobin, and the locus was called Sol ( Popp, 1962a). It was later shown that alleles at the same locus govern differences in tryptic peptides of the α-chain of the hemoglobin molecule. Hba is therefore probably the structural locus for the α-chain ( Popp, 1962b). It is not linked to Hbb, the probable structural locus for the β-chain. Hba alleles are classified on the basis of solubility, crystal shape, or peptide differences revealed by electrophoresis and chromatography ( Popp, 1965b; Hutton et al., 1964). At least four different alleles have been described. See also MGI.

Hbb locus, hemoglobin β-chain, I, Chapter 17. Called Hb when first discovered. Two codominant alleles are well established, Hbb^s which produces an electrophoretically single hemoglobin, and Hbb^d which produces a diffuse electrophoretic pattern with two distinct hemoglobins ( Ranney and Gluecksohn-Waelsch, 1955; Gluecksohn-Waelsch et al., 1957; E.S. Russell and Gerald, 1958; Popp, 1965b). The two hemoglobins produced by Hbb^d have different "β"-chains and both of these are somewhat different from the β-chain produced by Hbb^s (Hutton et al., 1962a, 1962b; Popp, 1962b). The Hbb locus is thought to be the structural locus for the β-chain and to be structurally complex, possibly duplicated in the Hbb^d allele. Morton ( 1962) has described a possible third allele, provisionally symbolized Hbb^p, which produces hemoglobin distinguishable from Hbb^d by minor electrophoretic differences. See also MGI.

Hc locus, hemolytic complement, linkage not known, Chapter 15. The locus was independently discovered by immunological methods and the antigen produced by Hc¹ was called MuB1 ( Cinader et al., 1964). Two alleles are known, Hc¹, found in strains DBA/1J, BALB/cJ, C57BL/6J, and others, which determines the presence of hemolytic complement in serum, and Hc⁰, found in strain DBA/2J, which determines the absence of detectable hemolytic complement in the serum ( Herzenberg et al., 1963b). Hc¹/Hc⁰ mice are indistinguishable from Hc¹/Hc¹. Absence of complement has no apparent effect on viability and does not reduce bacterial phagocytosis ( Stiffel et al., 1964). See also MGI.

hf, hepatic fusion, recessive, I. Discovered in the MA/MyJ inbred strain in which the mutant is homozygous. Homozygotes have varying degrees of fusion between the left portion of the central lobe and the adjacent left lateral lobe. Penetrance decreases on outcrossing, suggesting that the residual genotype of the MA strain is favorable for the complete expression of the gene. Similar fusion has not been discovered in other strains routinely autopsied at The Jackson Laboratory ( Bunker, 1959). See also MGI.

Hk, hook, semidominant, XVIII. Arose spontaneously in a piebald shaker stock. Homozygotes are viable and fertile, and at least on some genetic backgrounds are more severely affected than heterozygotes. Heterozygotes may not be detectably abnormal, or they may have shortened, crooked, or hook-shaped tails, and an abnormal anus. The anus tends to be slitshaped rather than round, and to be bare rather than surrounded by hair. It may be very much elongated and displaced toward the tail, sometimes running well out onto the tail ( Holman, 1951). See also MGI.

hl, hair-loss, recessive, VI. Arose spontaneously. Homozygotes show progressive degeneration of hair follicles over the entire body, loss of hair becoming obvious after about five weeks. Some specimens never lose all hair, others become very wrinkled and resemble rhino ( Hollander and Gowen, 1959). An interesting peculiarity of this mutant is that hl/+ offspring of hl/hl mothers have extremely fragile skeletons which break easily and lead to excessive mortality until the age of about 2 weeks. The antagonism is probably prenatal. It is not immunological. The suggestion has been made that hl/hl mice may maintain and require a smaller pool of calcium than normal mice. Their hl/hl offspring are able to obtain enough to satisfy their smaller requirement but their hl/+ offspring obtain too little ( Hollander, 1960). See also MGI.

Hm, hammer-toe, dominant, XVII. Found in a linkage cross. Homozygotes are viable and fertile. Both homozygotes and heterozygotes are characterized by feet in which the second phalanx of digits 2, 3, 4, and 5 is strongly flexed. All four feet are affected. Homozygotes have webbing between digits 2, 3, 4, and 5, extending to the nails in the hind feet and to the base of the distal phalanges in the forefeet. Heterozygotes also show webbing, but it usually does not extend so far on the toes ( Green, 1964b; Green and Kaufer, unpublished). See also MGI.

Hp, hairpin tail, probably semidominant, linkage not known. Arose in the AKR/J strain. Heterozygotes usually have a short kinky tail and abnormalities of the sacral, lumbar, and thoracic vertebrae, with most severe effects in the sacral region. Viability is reduced and females have small litters. Spermatogenesis is abnormal but males sire litters of about normal size. The fate of homozygotes is unknown ( Dickie, 1965). See also MGI.

hr locus, III. See also MGI.

hr, hairless, recessive, Figure 8-1G, Chapter 23. Found in a mouse caught in an aviary in London ( Brooke, 1926). Homozygotes develop a normal coat up to the age of about 10 days, at which time they begin to lose their hair. The complete hair is lost from the follicle. After a short time a few thin fuzzy hairs grow in but are soon lost. Waves of similar growth occur at intervals of about a month thereafter but the animals appear essentially hairless ( Crew and Mirskaia, 1931). The regenerating hairs come exclusively from guardhair (tylotrich) follicles, which are, however, very abnormal ( Mann and Straile, 1961). The vibrissae, which also grow from tylotrich follicles are repeatedly shed and become more abnormal with age. The toenails are excessively long and curved. Histologically there is a hyperkeratosis of the stratified epithelium and the upper part of the hair canals beginning at about 14 days. Hair club formation is abnormal and the lower part of the follicles tend to separate from the upper part. The isolated lower parts develop into cysts which become quite large and numerous ( David, 1932; Fraser, 1946). Some cysts arise from isolated sebaceous glands. Regardless of their origin all cysts at first undergo a sebaceous transformation and later a keratinization ( Montagna et al., 1952). Hairless mice are fertile but most females do not nurse their young well. See also MGI.

hr^rh, rhino, recessive. Arose as a spontaneous mutation in the descendants of a cross between two inbred lines. Homozygotes are similar to hr/ hr except that no hair regeneration occurs, and the skin becomes thickened and enormously wrinkled ( Howard, 1940). The hyperkeratosis in the hair follicles is very extensive, producing balls of keratin, utriculi, in such large numbers that the skin area is greatly increased. In addition, the subepidermal cysts are much larger than in hr/ hr ( Fraser, 1946). Rhino females do not nurse their young well. hr/hr^rh mice resemble hr/ hr but histologically are somewhat intermediate. The rhino condition is not cured by massive doses of vitamin A ( Mauer, 1961). Rhino skin when transplanted to normal hosts grows some hair around the edges, but this is probably due to the nonspecific effect of transplantation ( Tsuzi and Yosida, 1960). See also MGI.

hr^ba, bald, recessive. Arose spontaneously in a stock of albino mice of unknown origin. This allele is intermediate between hr and hr^rh in its effects ( Garber, 1952a). See also MGI.

Ht, hightail, semidominant, VI. Radiation-induced. Homozygotes die before birth. In heterozygotes the tail emerges high, is short and thick at the base, but is never kinked. Ht/+ mice are usually smaller than their normal littermates ( Gower, 1957). See also MGI.

hy-1, hydrocephalus-1 recessive, linkage not known, probably extinct. Discovered by Clark ( 1932). Penetrance is incomplete. Homozygotes with recognizable hydrocephalus usually die but a few reach maturity and breed. The abnormality is recognized externally as a dome-shaped head which may sometimes be seen at birth and in other case develops during the first 2 weeks ( Clark, 1934). Internally, the whole ventricular system is dilated, but the cause has not been determined ( Bonnevie and Brodal, 1946). See also MGI.

hy-2, hydrocephalus-2, recessive, linkage not known, probably extinct. Discovered by Zimmerman ( 1933) in the offspring of mice caught in the wild. Penetrance was reported to be complete and homozygotes never bred. Not allelic with hy-1 ( Clark, 1935). The anomaly resembles hy-1 but is more severe. See also MGI.

hy-3, hydrocephalus-3, recessive, linkage not known, Figure 8-1D. Found by inbreeding a heterogeneous stock of laboratory mice ( Grüneberg, 1943b). It has not been tested for allelism with hy-1 or hy-2. Penetrance is incomplete. Homozygotes with frank hydrocephalus die by 4 or 5 weeks of age. It seems likely that some apparently normal mice which survive and breed are hy-3/hy-3, but no pure breeding line in which all mating produce some hydrocephalus has been established. The lateral ventricles and the third ventricle are enlarged, the aqueduct of Sylvius and the fourth ventricle are only slightly affected, and there is some dilatation of the ventral subarachnoid cistern. The hydrocephalus seems to be due to a defect in the subarachnoid space caused by an abnormal postnatal differentiation of the arachnoid mater and the pia mater which prevents their separation ( Berry, 1961a). See also MGI.

hz, haze, recessive, linkage not known. Arose in the DBA/2 strain. In homozygotes the hair tips are brownish and the underfur is white. At birth the eyes are light colored ( Dickie, 1965). See also MGI.

ic, ichthyosis, recessive, linkage not known. Arose spontaneously in a sibmated stock. Homozygotes are recognizable at 2 days of age by their shorter vibrissae. The vibrissae become curved a day or so later. The first coat is delayed and is short, thin, and somewhat curly. During the third and fourth weeks the skin may develop scales. Sometimes these are large and hard and may reduce viability considerably. Often the tail has constrictions resulting in loss of the tip. Adults may be bare or may have a thin fuzzy coat. Viability and fertility are considerably reduced ( Carter and Phillips, 1950). Hairs of the coat are thin and wavy and have an unevenly compressed medulla with irregular distribution of melanin granules. The tail epidermis is thicker and more active than normal ( Spearman, 1960). See also MGI.

Id-1, isocitrate dehydrogenase-1 locus, linkage not known. This locus controls an electrophoretic difference in one of the three isocitrate dehydrogenases known to be present in mouse cells, namely the one that is specific for triphosphopyridine nucleotide (NADP) and is located in the soluble fraction of the cell. It migrates anodally on starch gel at pH 6.0. Two alleles are known; Id-1^a, controlling the slow migrating variant and found in strains C3H/HeJ, C57BL/6J, BALB/cJ and others, and Id-1^b, controlling the fast migrating variant and found in strains DBA/1J, DBA/2J, AKR/J, CBA/J and others. Id-1^a/Id-1^b mice have three electrophoretic forms, the two parental forms and a more abundant intermediate form. This suggests that the enzyme controlled by this locus is a dimer ( Henderson, 1965). See also MGI.

Ig-1 locus, immunoglobulin-1, Chapter 15. Linkage group not known, but closely linked to Ig-2. There is no agreement on the symbol to be used for this locus. Synonyms are: _γB^A ( Kelus and Moor-Jankowski, 1961), MuA2 ( Dubiski and Cinader, 1963), As_a ( Dray et al., 1963), Gg ( Wunderlich and Herzenberg, 1963; Herzenberg et al., 1963a), and Iga ( Mishell and Fahey, 1964). The terminology used here ( Herzenberg et al., 1965) is in conformity with that used for the histocompatibility loci. The antigenic activities controlled by this locus were demonstrated by preparing isoprecipitins in strains carrying one allele to γ-globulins from strains carrying another allele. The antigenic activity is found on the H chain of 7S _γ2a-globulin ( Mishell and Fahey, 1964; Fahey et al., 1964). At least eight codominant alleles are known ( Lieberman and Dray, 1964; Herzenberg et al., 1965). In Herzenberg's classification the alleles and strains they occur in are: Ig-1^a in C3H/HeJ and BALB/c; Ig-1^b in C57BL/10J; Ig-1^c in DBA/2J and DBA/1J; Ig-1^d in AKR/J; Ig-1^e in A/J; Ig-1^f in CE/J; Ig-1^g in RIII/J; and Ig-1^h in SEA/Gn and BDP/J. See also MGI.

Ig-2 locus, immunoglobulin-2, linkage not known, but very close to Ig-1, Chapter 15. This locus specifies antigens on the H chain of the _β2A-globulin. Two alleles have been identified directly, one in C3H/HeSn and the other in DBA/2J. At least one other allele remains to be identified, as a number of strains have neither the C3H or the DBA/2 antigen ( Herzenberg, 1964).

The antigenic specificity of a third immunoglobulin has been shown to be controlled by a locus very closely linked to Ig-1 or identical to it ( Lieberman et al., 1965). The specificity is found on the H chain of the 7S globulin called _γ in the terminology of Fahey et al. ( 1964) or _γG-Be2 in the terminology of the authors. Different alleles are present in the BALB/c and C57BL/6 strains. See also MGI.

iv, situs inversus viscerum, recessive, linkage not known. Arose spontaneously in a noninbred stock ( Hummel and Chapman, 1959). Penetrance is incomplete, 71 per cent in the stocks examined. Homozygotes may show left-right transposition of thoracic and abdominal viscera and associated blood vessels, anomalous relationships of postcaval and azygous veins, anomalous position of the hepatic portal vein, abnormalities in spleen position and shape, and abnormalities in liver and lung lobation. See also MGI.

j, jaw-lethal, recessive, linkage not known, probably extinct. Found in the descendants of both irradiated and control mice by Little and Bagg ( 1924). Homozygotes are stillborn, death resulting from abnormalities of the head including shortening of the head, reduced or absent lower jaw, microphthalmia, anophthalmia or cyclopia, abnormal or missing tongue, lack of opening between oral and nasal passages and the trachea and pharynx, and various abnormalities of the brain ( Johnson, 1926). See also MGI.

ja, jaundiced, recessive, linkage not known, Chapter 17. Arose in the 129 inbred strain. Homozygotes are anemic at birth and become jaundiced within a few hours. The anemia is present in 15-day fetuses. Examination of the blood of jaundiced mice shows that they have a severe microcytic anemia with about half the normal number of red cells. There is considerable erythrocyte destruction and a compensating release of immature cells into the blood. Homozygotes die within a day or two of birth ( Stevens et al., 1959). See also MGI.

je, jerker, recessive, linkage not known ( Wallace, 1958a), Chapter 32. Originated as a dancing mouse found by a fancier and given to Grüneberg ( Grüneberg et al., 1941). Homozygotes show the typical behavior of the circling mutants, head-tossing, circling, hyperactivity, and deafness. The abnormal behavior is associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus ( Deol, 1954). See also MGI.

jg, jagged-tail, recessive, XVII. Arose spontaneously in the C3H/HeJ inbred strain. Homozygotes have tails with a normal tapering tip but usually much shortened and kinked. In the most severely affected individuals other parts of the vertebral column may be abnormal; in the less severely affected it appears nearly normal. Testes are much reduced in size and the males are probably sterile. Females have small ovaries. They may breed but litters are few and small. Viability of both sexes is considerably reduced ( Green, 1964a). See also MGI.

ji, jittery, recessive, X. Discovered by DeOme ( 1945) as a spontaneous mutation in the Bagg albino strain. Homozygotes usually die by 4 weeks of age. They show muscular incoordination beginning at 10 to 16 days. Epileptiform seizures follow within a few days. As seizures and incoordination become more severe the mice lose ability to obtain food and die apparently from starvation and thirst. Polycystic alterations in the white matter of the brain have been reported ( Harman, 1950). See also MGI.

jo, jolting, recessive, linkage not known. Arose in the DBA/2WyDi strain. Homozygotes shiver or quake in the anterior part of the body and show some incoordination of the hind limbs. They often survive to adulthood and some have bred ( Dickie, 1965). See also MGI.

jp, jimpy, recessive, XX (Sex linked), Chapters 15, 32. Arose spontaneously in an inbred line. Hemizygous males die between 20 and 40 days of age. Homozygous females cannot therefore be produced. Affected males appear normal when sitting quietly, but beginning at about 2 weeks they show a marked tremor when attempting movement. The tremor is most noticeable in the hindquarters. From 3 weeks on convulsions may occur ( Phillips, 1954). The central nervous system is very deficient in myelin. Cells of certain white matter tracts contain nonpolar lipids in the form of strongly sudanophilic cytoplasmic granules. Impaired myelin formation appears to be accompanied by formation of an abnormal lipid resulting from abnormal myelin synthesis or from myelin destruction ( Sidman et al., 1964). See also MGI.

jt, joined-toes, recessive, linkage not known. Arose spontaneously in the 129 inbred strain. Homozygotes show fusion of the soft tissue of the digits, more commonly on the hind feet than on the forefeet. Fusions are more common between the second and third, and third and fourth digits, but all five may be involved ( Stevens, 1955, as "syndactylism"). See also MGI.

kd, kidney disease, recessive, linkage not known. Found in the CBA/H strain. Homozygotes develop nephrosis recognizable at the age of 2 to 3 months when urine becomes pale or colorless. Affected animals can produce two or three litters before becoming ill ( Hulse et al., 1965). See also MGI.

kr, kreisler, recessive, V. Found by Hertwig ( 1942) in the descendants of an irradiated male. Viability and fertility are less than normal. Males are more likely to breed than females. In homozygotes both the bony and membranous labyrinths are very abnormal. The abnormality traces back to faulty segmentation of the neural tube in the region of the rhombencephalon in 8 ¾-day embryos, followed by degeneration of cells in the fourth rhombomere ( Deol, 1964a). The abnormalities of the neural tube are thought to lead to an abnormal position of the ear vesicles which in 9-day kreisler embryos are not directly in contact with the neural tube as they are in normal embryos. An imperfect capsule forms around the vesicle and extracapsular cysts result from growth of the vesicle through gaps in the capsule. The cysts are often quite large and located under the brain ( Hertwig, 1944; Deol, 1964a). The abnormal behavior resulting from these defects is very similar to that of the degenerative group of circling mutants. See also MGI.

Kw, kinky-waltzer, dominant, or semidominant, linkage not known. Probably radiation induced. Heterozygotes are viable and fertile. Penetrance is incomplete in heterozygotes. No description of homozygotes has been published. In heterozygotes the amount of kinking of the tail is variable and may or may not be accompanied by a balance defect. The balance defect has not been seen without the kinky tail ( Gower and Cupp, 1958, as "kinky tail balance defect"). This mutant resembles Q, Fu, and Fu^ki but tests for allelism have not been reported. See also MGI.

la, leaner, recessive, linkage not known. Arose spontaneously in the AKR/J strain ( Dickie, 1962b, as "heeler"). Most homozygotes survive and can breed. They are recognizable at 10 days of age. Adults show instability of trunk and altered muscle tone in trunk and limbs. They have degenerative changes affecting virtually all neuron types in a patchy distribution in the cortex of the vermis of the cerebellum. The distribution of the disorder within the cerebellum accounts for the more severe ataxia in the trunk than in the limbs, in contrast to the ataxia of rl, sg, and wv, which have malformations affecting the cerebellar cortex more diffusely ( Sidman, 1965). See also MGI.

Lc, lurcher, semidominant, XI. Arose as a spontaneous mutation in a male homozygous for white ( Mi^wh). Heterozygotes show a characteristic swaying of the hindquarters during which they fall to one side or the other. There is no trembling but a jerky up and down movement, particularly in older mice. They are identifiable with sureness at 12 to 14 days of age. Homozygotes die shortly after birth but have no visible abnormalities. Heterozygotes are smaller than normal at maturity. Males are fully fertile but the litter size of heterozygous females is reduced about one-quarter ( Phillips, 1960a). See also MGI.

ld, limb deformity, recessive, Chapter 15. Arose at Oak Ridge National Laboratory, possibly radiation induced. Homozygotes have reduced viability but often live and breed. Skeletal deformities appear to be confined to the portions of the limbs below the elbow and knee. The radius and ulna appear to be fused into a broad flat bone; the tibia and fibula are replaced by a short bone, usually triangular. The fore and hind feet are radically reduced and disorganized ( Cupp, 1960). A similar mutation at the same locus occurred at The Jackson Laboratory. The tibia and fibula are replaced by a single long bone in homozygotes of this allele, and the viability appears to be lower. Whether the difference is an effect of the residual genotype or due to a real difference in the alleles is not known ( Green, 1962; Cupp, 1962). See also MGI.

le, light ears, recessive, XVII. Arose spontaneously in the C3H/HeJ strain. Closely resembles ep. Homozygotes have light ears, tail, and feet, and a slightly diluted juvenile coat which becomes darker in the adult. Eyes are pale at birth and darken with age (Lane and E.L. Green, 1965, personal communication). See also MGI.

lg, lid gap, recessive, linkage not known. Spontaneous. Homozygotes are viable ( L.B. Russell, 1961). A repeat mutation at this locus occurred at the University of British Columbia and was studied by Watney and Miller ( 1964). Penetrance is incomplete. About 70 per cent of homozygotes have one or both eyes open at birth. Cortisone administered to the mother on the 15th day of pregnancy reduces the incidence of the defect in homozygotes to zero ( Chapter 14). lg is not allelic with gp and oe, and has not been tested for allelism with lo ( Miller, 1964). See also MGI.

lh, lethargic, recessive, linkage not known, Figure 8-2H. Arose spontaneously in the BALB/cGn strain. Homozygotes make long pauses between movements, often hunch the back, and may raise first a front foot and then a hind foot. They may sit up with the front feet contracted for several minutes. Both sexes breed and there is little early mortality ( Dickie, 1964b). See also MGI.

ln, leaden, recessive, XII, Chapter 21. Arose spontaneously in the C57BR inbred line ( Murray, 1933). In its effect on coat color ln is indistinguishable from d. Like d it causes clumping of melanin granules into larger masses, but no change in color of the pigment. The clumping is due to the shape of the melanocytes, which have fewer and thinner dendritic processes than wild-type melanocytes with the result that the pigment granules are largely clumped around the nucleus ( Markert and Silvers, 1959). See also MGI.

lo, lids open, recessive, linkage not known. Arose spontaneously. Homozygotes are viable ( Saylors, 1961). Tests for allelism with other similar mutants ( gp, lg, oe) have not been reported.

Lp, loop-tail, semidominant, XIII, Figure 8-2B. Discovered by Strong and Hollander ( 1949) as a spontaneous mutation in the A strain. Lethal when homozygous, probably not fully penetrant in heterozygotes. Heterozygotes have looped or crooked tails and often show a wobbling of the head. In females the vagina may be imperforate. Homozygotes have open neural folds in the region of the brain and may or may not have open spinal cords as well. They are usually alive until birth but never survive thereafter ( Strong and Hollander, 1949). The axial skeleton and ribs of homozygotes are abnormal, apparently as a secondary result of the abnormalities of the nervous system ( Stein and Mackensen, 1957). In Lp/Lp embryos of 9 to 9 ½ days, the shortening or regression of the primitive streak is retarded and the neural plate and notochord are shorter than normal. Failure of the neural tube to close apparently results from its failure to elongate ( Smith and Stein, 1962). See also MGI.

lr, lens rupture, recessive, linkage not known, Chapter 29. Arose spontaneously in an inbred strain albino strain ( Fraser and Herer, 1948). Penetrance is complete on some genetic backgrounds, but may be reduced on others. In homozygotes, beginning at about 3 weeks of age there is cataractous degeneration of the lens with rupture of the capsule and expulsion of the lens nucleus into the vitreous chamber. The lens shrinks, tearing the suspensory ligaments, and may pass through the pupil into the anterior chamber ( Fraser and Herer, 1950). This mutant resembles ec but has not been tested for allelism with it. See also MGI.

ls, lethal spotting, recessive, V, Chapters 15, 21, 29. Arose in a subline of an inbred strain, C57BL- a^t. Homozygotes resemble piebald mice ( s/ s) in having considerable white spotting. They die usually in the third week of life with megacolon associated with lack of ganglion cells in the lower colon ( Lane, 1966). The mutant seems to exert its effect on pigmentation by reducing the number of melanoblasts, possibly through an effect on the neural crest ( Mayer and Maltby, 1964). See also MGI.

lst, Strong's luxoid, semidominant, linkage not known, Chapters 15, 29. Arose in a line treated with methylcholanthrene for 22 generations ( Strong and Hardy, 1956). Heterozygotes show preaxial abnormalities of the hind feet, including polydactyly and triphalangy of the hallux. Very rarely the forefeet may also be affected. Penetrance is incomplete and dependent on the genetic background. Homozygotes show preaxial polydactyly of all four feet, reductions and duplications of the radius, reductions and rarely duplications of the tibia, reduction of the pubis, modifications of the skull, temporary dorsal alopecia, a posterior shift of the umbilicus ( Forsthoefel, 1962), and a temporary postnatal anemia due to bleeding at the umbilicus ( Kuharcik and Forsthoefel, 1963). There is no effect on the number of ribs, presacral vertebrae, or sternebrae in either heterozygotes or homozygotes. Males are sterile but females sometimes breed. Forsthoefel ( 1963) found that embryonic development of parts of the limbs, head, integument, and belly is retarded. See also MGI.

lt, lustrous, recessive, linkage not known. Arose in the DBA/2J strain. The fur of homozygotes has a very satiny appearance and the vibrissae are curly. Not allelic with satin ( Dickie, 1965). See also MGI.

lu, luxoid, semidominant, II, Figure 8-1E, Chapters 14, 15. Arose spontaneously in the C3H/He inbred strain ( Green, 1955). Heterozygotes show preaxial polydactyly or hyperphalangy of the hind feet. Penetrance is close to zero in the C3H/He strain and about 90 per cent in the C57BL/10 strain. Homozygotes show preaxial polydactyly, hyperphalangy, or oligodactyly of the hind feet, preaxial polydactyly or hyperphalangy of the forefeet, tibial hemimelia, and occasionally radial hemimelia and tail kinks. The gene tends to increase the number of presacral vertebrae, ribs, sternebrae, and total number of vertebrae, the effect being greater in homozygotes than in heterozygotes. Males are sterile but an occasional female may breed ( Forsthoefel, 1958). The developmental effects of lu in homozygotes can be traced back to the 10 ½-day stage when the posterior end of the coelom is found to be more caudal than in normal controls. The somites of the tail may be abnormal, and there are more somites than in controls. An increased rate of growth along the longitudinal axis with some loss of orderly control is proposed as a possible explanation of the axial anomalies. How the limb abnormalities are related to the axial abnormalities is not clear ( Forsthoefel, 1959). A very similar mutant has been described by Kobozieff and Pomriaskinsky-Kobozieff ( 1962 and earlier). It has not been tested for allelism with lu. See also MGI.

Lv locus, levulinate dehydratase, XIV, Chapter 19. An interstrain difference in the hepatic activity of δ-aminolevulinate dehydratase is controlled by this locus. Two alleles have been described, Lv^a for high activity (in strain AKR/J) and Lv^b for low activity (in strain C57BL/6J). The enzyme effects the condensation of two molecules of δ-aminolevulinate to form porphobilinogen. Lv^b/Lv^b mice have lower levels of enzyme than Lv^a/Lv^a mice at all stages from 8 days before birth to adulthood. Heterozygotes are intermediate ( R.L. Russell and Coleman, 1963). See also MGI.

lx, luxate, semidominant, XVII, Chapter 15. Found in descendants of a silver mouse obtained from a fancier ( Carter, 1948). A similar mutant had been reported by Rabaud (1914; see Grüneberg, 1952, for description) but is extinct and cannot now be tested for allelism with lx. Heterozygous lx/+ mice show preaxial polydactyly (including hyperphalangy of the first digit) of the hind feet. Penetrance is incomplete and dependent on the genetic background. Homozygotes show preaxial polydactyly or oligodactyly of the hind feet, reduction of the tibia, loss of part of the femur and pubis, decrease in the number of presacral vertebrae, and anomalies of the urogenital system including horseshoe kidney, hydronephrosis, and hydroureter (Carter, 1951c, 1953). The abnormalities of homozygotes can be traced back to the 10-day stage when the posterior end of the coelom is nearly a full segment anterior to its position in normal sibs. A day later the right umbilical artery is highly abnormal and, with the left umbilical artery, forms a ring which is often too small to allow free passage of the developing kidneys as they migrate forward. The posterior limb buds of homozygotes are narrower than normal from a very early stage ( Carter, 1954). The hind limb bud, the umbilical arteries, and the posterior end of the coelom are all close together in the 10-day embryo, but the causative relationship between the abnormalities of the three parts is not clear. See also MGI.

m, misty, recessive, VIII. Arose spontaneously in the DBA/J inbred strain. Homozygotes are lighter in color than normal and usually have a white belly spot and tail tip. The color of m/m mice is not so diluted as that of d/ d or ln/ ln, and the hairs of the coat have more cortical pigment than in d/ d or ln/ ln (Woolley, 1941, 1945) See also MGI.

ma, matted, recessive, XVI. Arose spontaneously in the CBA/Gr inbred strain. Homozygotes can first be identified between 2 and 4 week of age. The hairs are more erect than normal and are matted in clumps, there is a tendency to baldness depending on areas of friction and resulting hair breakage, and a color change to russet happens toward the end of each hair cycle in black hair. Hairs are normal in morphology, but are brittle and tend to split longitudinally. Viability and fertility are normal ( Searle and Spearman, 1957). The defect in matted hairs is thought to be in the cuticle ( Jarrett and Spearman, 1957). See also MGI.

mc, marcel, recessive, linkage not known. Arose in the C57BL/10 strain. Homozygotes have pronounced waves in the coat at 14 to 21 days. Female homozygotes are sterile. Not allelic with we, wa-1, or wa-2 ( Foerster, 1956). See also MGI.

md, mahoganoid, recessive, linkage not known. Arose in the C3H/HeJ inbred strain. This gene is identical to mahogany ( mg) in its effects on the coat color of A/- and a/ a mice. The two mutants are neither allelic nor linked ( Lane, 1960a). See also MGI.

mdg, muscular dysgenesis, recessive, linkage not known, Chapter 29. Arose spontaneously in a tailless line. Homozygotes never develop normal skeletal muscle. The first observable effects occur at 13 days of gestation when there is marked edema and at the same time failure of myoblasts to differentiate into striated myotubes. Subsequently all skeletal muscle cells degenerate. At birth the thorax and limbs are almost bare of muscle. Cardiac and smooth muscle as well as nervous tissue are normal. There are numerous skeletal abnormalities, including a short lower jaw and usually a cleft palate, which may be secondary to the abnormalities of muscle. Homozygotes do not survive birth ( Gluecksohn-Waelsch, 1963; Pai, 1965). See also MGI.

mg, mahogany, recessive, V. Appeared in an agouti stock of unknown origin. In homozygous condition mg darkens the back, ears, and tail of agouti mice and darkens the ears and tail of nonagouti mice. a/ a mg/mg mice resemble a^e/ a^e ( Lane and Green, 1960). See also MGI.

mi locus, XI, Chapters 21, 29. See also MGI.

mi, microphthalmia, semidominant. Found among the descendants of an irradiated male ( Hertwig, 1942). In heterozygotes the eyes have less iris pigment than normal, both at birth and throughout life ( Grüneberg, 1948). Heterozygotes may also show white spotting on the belly, head, and tail. Homozygotes are devoid of pigment in the hair and eyes. The eyes are very small usually with cataracts ( Tost, 1958) and the eyelids never open. Most homozygotes die at about weaning. There is a failure of secondary bone absorption, as in grey-lethal but a little less severe ( Grüneberg, 1948; Freye, 1956). During development the optic vesicle fails to form a proper cup and the choroid fissure remains permanently open (Müller, 1950, 1951). See also MGI.

mi^bw, black-eyed white, recessive to wild type. Arose spontaneously in the C3H inbred strain. Homozygotes have white coats and black eyes. Occasionally a few pigmented hairs may be found on the back ( Kreitner, 1957). Melanoblasts cannot be demonstrated in the skin of embryos of these mice by transplantation to the eyes of albino hosts ( Markert, 1960). Mi^wh/mi^bw mice have pigmented eyes and are white with some pale yellow spots which become white in the adult ( Schaible, 1963c). See also MGI.

mi^sp, mi-spotted. Found in a C57BL/6J- Mi^wh stock. Homozygotes and mi^sp/+ are not detectably different from +/+ in color but have slightly less tyrosinase activity in the skin; Mi^wh/mi^sp are light yellow with dorsal and ventral white spots and pigmented eyes. Medullary pigment granules show much clumping and are yellowish brown ( Wolfe and Coleman, 1964). mi/mi^sp mice are white with some pigmentation in the eyes and some flecks of pigmented hair on the back. All these combinations are viable and fertile ( Wolfe and Coleman, 1964). See also MGI.

Mi^wh, white, semidominant. Found among offspring of a cross between the DBA and C57BL strains ( Grobman and Charles, 1947). Heterozygotes are somewhat lighter than d/ d mice and have light ears. They may also have a white belly spot and rarely a dorsal spot. Medullary pigment granules in the hairs appear to vary greatly in size and shape, apparently because of clumping ( Wolfe and Coleman, 1964). Homozygotes are white with very slightly pigmented eyes. They have no pigment cells except a few in the retina ( Markert and Silvers, 1956). They are slightly microphthalmic and are usually smaller and less fertile than normal. Mi^wh/ mi are also white. They have slightly pigmented eyes, normal skeleton, and are slightly less microphthalmic than Mi^wh/Mi^wh (Grüneberg, 1952, 1953c). See also MGI.

mi^ws, white spot, semidominant. Arose in the C57BL/6 strain. mi^ws/+ mice have a white diamond on the belly. mi^ws/mi^ws are all black-eyed white. Mi^wh/mi^ws are white with some dark patches and dark eyes ( Miller, 1963; Hollander, 1964). See also MGI.

mk, microcytic anemia, recessive, linkage not known, Chapter 17. Arose spontaneously in a hybrid stock. Homozygotes are pale at birth and slightly smaller than normal. The red blood cells are extremely microcytic. At birth the number of red blood cells is slightly less than normal but rises so that by 8 weeks of age it may be one and two-thirds times normal. During the first week of life some homozygotes show an extreme scaliness of the skin. Only about 50 per cent of homozygotes survive to weaning ( Nash et al., 1964). See also MGI.

mn, miniature, recessive, probably VI. Appeared in the descendants of an outcross of AKR to a stock at Columbia University. Homozygotes are smaller than their normal sibs at birth and have a dorsoventral flattening of the skull. They grow more slowly and are only about one-fourth to one-third normal size at 75 days. They do not seem to differ much from normal in body proportions or in other anatomical features or behavior, but mortality is high at all times up to 2 months when 96 per cent were dead ( Bennett, 1961b). See also MGI.

Mo locus, XX (sex-linked). Mutations at the Mo locus seem to be very common. Mutations at the Mo locus seem to be very common. Numerous mutations similar in phenotype have been reported, and although allelism is difficult to prove in this case, it is likely that most of them are remutations at this locus ( Lyon, 1960; Welshons and Russell, 1959). See also MGI.

Mo, mottled, semidominant, Chapter 15. Arose spontaneously in a cross segregating for several color factors ( Fraser et al., 1953). Heterozygous females have irregular patches of full colored and very lightly colored fur over the whole coat. Patches with well-defined edges very rarely cross the middorsal or midventral line. Vibrissae are curly but the coat is not waved. Viability is reduced, some heterozygotes dying prenatally and some postnatally. Survivors are usually fertile. Hemizygous males die in utero at about 11 days of gestation with no visible abnormality ( Falconer, 1953). See also MGI.

Mo^br, brindled, semidominant. Arose spontaneously in the C57BL inbred strain ( Fraser et al., 1953). Heterozygous females are very similar to Mo/+ females in appearance but have normal viability. Hemizygous males are almost devoid of pigment except in the eyes and ears. The vibrissae are strongly curled and the coat is wavy. Males usually die when 2 weeks old but a few have lived and been fertile. They have a behavioral abnormality consisting of slight tremor, uncoordinated gait, and clasping of the hind feet when held up by the tail. These males have been used to produce Mo^br/Mo^br females which are identical in phenotype to hemizygous males. Mo/Mo^br females are indistinguishable from Mo^br/Mo^br females and Mo^br/Y males and die at the same age ( Falconer, 1956). See also MGI.

Mo^dp, dappled, semidominant. Arose in a low-dosage γ-irradiation experiment. Heterozygous females are similar in color and curliness of vibrissae to Mo/+ females. Some have clubbing of the forefeet at birth or, at weaning, a tendency to walk on the dorsal surfaces of the hind feet. With age, calcified lumps may appear in the region of the periosteum of the thoracic and lumbar vertebrae. Hemizygous males fie at about 17 days of gestation. They show bending and thickening of the ribs and distortion of the pectoral and pelvic girdles and limb bones ( Phillips, 1961). See also MGI.

mr, maroon, recessive, linkage not known. Arose spontaneously in a "lactation" stock. Eyes are colorless at birth, but darken to a rich maroon. The coat color varies from near normal to extreme pallid, even among littermates and darkens with age. Not allelic with d, ln, p, pa, or ru and interacts with si in the F₁. May be an allele of si ( Bateman, 1957). See also MGI.

mu, muted, recessive, linkage not known. Arose in a stock of t-alleles. Homozygotes have light eyes at birth and fur of a muted brown shade, often with white underfur. Some have a balance defect, similar to that of pa, which is due to absence of otoliths in one or both ears. Not allelic with pa ( Lyon and Meredith, 1965). See also MGI.

Mx, myxovirus resistance, dominant, linkage not known. Strain A2G is resistant to intracerebral inoculations of neurotropic influenza A virus, and strains A/J and CeH/HeJ are susceptible. In crosses between A2G and the other two strains, resistance segregated as if controlled by a dominant gene at a single locus ( Lindenmann, 1964). See also MGI.

my, blebs, recessive, linkage not known. Found among the descendants of irradiated mice ( Little and Bagg, 1923). Effects are variable and penetrance is incomplete. This mutant has been the subject of a large number of investigations reviewed by Grüneberg ( 1952). The genetics and development were reinvestigated by Carter ( 1956, 1959b) who concluded that the effects of my include: embryonic subepidermal blebs leading to abnormalities of the eyes, skin, and hair, clubbing of the feet, ectopic viscera, and split sternum; pseudencephaly, acrania, renal agenesis, preaxial polydactyly, and syndactyly of the middle digits; and probably also hydronephrosis, ectopia viscerum, and midcerebral lesions. See also MGI.

N, naked, semidominant, VI. Arose as a spontaneous mutation in a stock at the Latvian University of Riga ( Lebedinsky and Dauwart, 1927). Heterozygotes grow a nearly normal first coat. At 10 to 14 days the hairs begin to break off because of weakness due to incomplete keratinization. Breaking off and regeneration occurs in cycles and produces animals with irregular bare and haired patches which change as the cycle progresses. Heterozygotes are viable and fertile. Homozygotes lack vibrissae at birth. They often die before 10 days but some live and even breed. The effect on the coat is much more severe than in heterozygotes. Homozygotes never grow a complete coat. They have cycles of hair regeneration and loss, but the new hairs break off almost as soon as they are formed ( David, 1932; Fraser, 1946). See also MGI.

Nil, neonatal intestinal lipidosis, semidominant, I. Discovered in the A/Cam strain. Heterozygotes and homozygotes are classifiable at 0 to 5 days of age by the presence of white lipid in the wall of the small intestine visible through the skin. There is no milky fluid in the peritoneum. Expression is variable. Heterozygotes have variable penetrance, and homozygotes have greater expression and less viability than heterozygotes (Wallace, 1963a, 1965). See also MGI.

nu, nude, recessive, VII. Found in mice in the Virus Laboratory, Ruchill Hospital, Glasgow. Homozygotes do not grow even a first coat of hair and most die within a few weeks of weaning ( Isaacson and Cattanach, 1962). See also MGI.

ob, obese, recessive, XI, Figure 8-1A, Chapters 19, 20, 23, 29, 33. Arose as a spontaneous mutation in a multiple recessive stock ( Ingalls et al., 1950). Homozygotes are first recognizable at about 4 weeks. They increase in weight rapidly and may reach three times the normal weight. Females are always sterile but an occasional male may breed, particularly if maintained on a restricted diet. Obesity is due to a moderate hyperphagia and to marked inactivity. There is a moderate hyperglycemia which is not due to lack of insulin but probably to insulin insensitivity. There is increased secretion of insulin and hyperplasia of the islets of Langerhans. Incorporation of acetyl-CoA into fatty acids in adipose tissue is increased and lipolysis of tissue-triglycerides is depressed. Storage of fat and its nonutilization is thus favored ( Christophe, 1963; see also Mayer, 1960). See also MGI.

oe, open eyelids, recessive, VII. Arose spontaneously in inbred strain 129/RrSv. Not allelic with gp but has not been tested for allelism with lg and lo. Homozygotes have open eyelids at birth. The cornea usually becomes opaque in adults, and the eyes are usually smaller than normal. A corneal staphyloma may be present. Homozygous embryos can be distinguished at 17 days when the eyelids normally close. Some homozygotes at this stage have a protruding lens, folded retina, and constricted cornea ( Mackensen, 1960). See also MGI.

oel, open eyelids with cleft palate, recessive, linkage not known. Appeared in a phocomelic strain. Homozygotes have cleft palates and die soon after birth ( Gluecksohn-Waelsch, 1961). See also MGI.

ol, oligodactyly, recessive, I, Chapter 15. Appeared among the descendants of an X-rayed male (Hertwig, 1939, 1942). Homozygotes show reduction of the postaxial digits of all four limbs in varying degrees of severity. There may also be reduction or absence of the ulna and fibula. The tail may be shortened and kinked, the last rib is reduced in size or absent, and the ribs and sternebrae may show fusions. The spleen may be reduced in size and deformed, and there may be horseshoe kidney or the kidneys may be cystic or absent ( Freye, 1954). Few homozygotes live beyond 1 month. Survivors are small and do not breed. See also MGI.

or, ocular retardation, recessive, linkage not known. Appeared in a stock segregating for patch ( Ph) ( Truslove, 1962). Homozygotes have small eyes at birth and can be easily classified. The eyes develop normally up to the age of 11 days of gestation. After that they are smaller than normal because of the failure of the central artery and vein to establish a pathway along the choroid fissure, which closes completely. In the adult there is no optic nerve or optic chiasma. The space between the small eyeball and the orbit of normal size is filled with hypertrophied Harderian and lacrymal glands ( Truslove, 1962; Konyukhov et al., 1962). Eyes of or/or embryos cultured in the anterior chamber of eyes of adult mice develop a more normal lens that when left in situ ( Konyukhov et al., 1963). See also MGI.

Os, oligosyndactylism, semidominant, XVIII, Figure 8-1F, Chapters 15, 29. Arose in an irradiation experiment and was probably X-Ray-induced. Homozygotes die early in embryonic life but have not been described. Heterozygotes are affected on all four feet. Fusion usually occurs between the second and third digits and occasionally involves the fourth ( Grüneberg, 1956). The muscles of the forearms and lower legs as well as of the feet show anomalous arrangements not necessarily correlated with the skeletal changes ( Kadam, 1962). At 11 days of gestation the preaxial border of the limbs can be seen to be reduced ( Grüneberg, 1961a) and histological examination at this time shows that there is cellular degeneration of the preaxial part of the apical ectoderm ( Milaire, 1962). Os/+ mice have a mild diabetes insipidus present at 5 weeks and increasing with age ( Falconer et al., 1964). See also MGI.

p locus, I, Chapter 21. See also MGI.

p, pink-eyed dilution, recessive. This is a very old mutant carried in many varieties of fancy mice. Homozygotes have pink eyes with pigmentation very much reduced but not completely absent. The black pigment of the hair is very much diluted but the yellow pigment is only slightly affected. Pigment granules are irregular and shredlike in shape ( E.S. Russell, 1949a). Numerous recurrences of this mutation have been noted. One, which appears identical with p/p when homozygous, undergoes reverse mutation at the rate of about 0.3 per cent ( Wolfe, 1963b). See also MGI.

p^d, dark pink eye, recessive. Probably X-ray-induced. Eyes of homozygotes are slightly pigmented at birth and darken in the next few days; the coat is only slightly diluted. Eyes of p^d/ p mice are colorless at birth but darken during the first 2 weeks; the coat is diluted but darker than that of p/ p ( Carter, 1959a). See also MGI.

p^r, Japanese ruby, recessive. Discovered in a stock of Japanese waltzers ( Sô and Imai, 1926). The eyes of homozygotes are very variable in color and may be different on the two sides of the same animal. Coat color is intermediate between wild type and p/ p. p^r/ p mice resemble p/ p. This mutant may be extinct. See also MGI.

p^s, p-sterile, recessive. Probably X-ray-induced. This mutant is like p in its effect on pigmentation, but homozygotes are small and males are almost completely sterile. Females may be fertile but are poor mothers. Both sexes show slightly uncoordinated behavior and have incisors that wear abnormally ( Hollander et al., 1960). See also MGI.

pa, pallid, recessive, V. Found in a mouse caught in the wild ( Roberts, 1931). Eyes of homozygotes are pink and the coat is a little lighter than that of p/ p. Both black and yellow pigment are diluted. Homozygotes have slightly reduced viability and some have slightly abnormal behavior. The head is held tilted to one side or the other, and the mice may be unable to orient themselves if submerged in water. The abnormal behavior is due to the absence of otoliths in the sacculus and utriculus which occurs in many but not all pa/pa mice. See also MGI.

pc, phocomelic, recessive, linkage not known, Chapter 15. Found in a tailless stock. Homozygotes show disproportionate dwarfism and die shortly after birth as a result of a large median cleft palate. The skull is narrow and pointed, the upper incisors are small or absent, and the limbs are disproportionately shortened. Both polydactyly and syndactyly may occur ( Gluecksohn-Waelsch et al., 1956). Embryos show retardation of precartilage formation in the limbs and head at 12 days of gestation, and chondrification and ossification of the extremities is retarded throughout development ( Sisken and Gluecksohn-Waelsch, 1959; Fitch, 1957). Extra pieces of cartilage are often found in the head and limbs. Two abnormal bars of cartilage in the area where palatine closure normally occurs are thought to interfere mechanically with closure. See also MGI.

Pd locus, pyrimidine degrading, linkage not known, Chapter 19. Two alleles are known at this locus: Pd^a produces a low level of pyrimidine degrading enzyme activity (in strains C57BL/6J and BDP/J); Pd^b produces a high level (in strains SJL/J and RF/J). Three enzymes are affected simultaneously; they catalyse the stepwise reactions uracil --> dihydrouracil --> β-ureido-propionic acid --> CO₂ + NH₃ = β-alanine. If the rate of reaction is measured by determining the radioactivity of respiratory CO₂ after injection of radioactive uracil, Pd^b is fully dominant to Pd^a. If the same reaction is carried out with liver slices, Pd^a/Pd^b is intermediate between the two homozygotes ( Dagg et al., 1964). See also MGI.

pe, pearl, recessive, XIV, Chapter 21. Arose spontaneously in the C3H/He inbred strain. Homozygotes have a smaller amount of pigment in the eyes at birth than normal, but the eye color cannot be distinguished from normal in adults. The yellow and black pigments are diluted. Viability until maturity is good, but females have a tendency to die during pregnancy and lactation and the survivors are poor mothers ( Sarvella, 1954). Somatic reverse mutation to wild type are frequent, but the frequency is different on different genetic backgrounds ( L.B. Russell and Major, 1956). See also MGI.

pf, pupoid fetus, recessive, VIII. Found among the fetuses of dissected pregnant females in an irradiation experiment. Homozygotes die at birth. The skin of late fetuses is stretched in an anteroposterior direction and lacks hair follicles. Fore and hind limbs and tail are seen as smooth stubs covered and held bound to the body by an abnormal epidermis. The cartilaginous skeleton appears grossly normal ( Meredith, 1964). See also MGI.

pg, pygmy, recessive, IV. Appeared as undersized segregants in a strain selected for small size ( MacArthur, 1944). Homozygotes are recognizably smaller than normal at birth. Their growth rate is low and they weigh about one-third as much as normal when adult ( King, 1950). They are healthy and active but some are sterile. Fertility may be almost normal on genetic backgrounds favoring large size. The dwarfing is not due to a pituitary deficiency, and the thyroid and adrenals appear normal ( King, 1955). The gene increased in frequency during five generations of selection for small size, indicating that pg probably reduces the size of heterozygotes ( Warwick and Lewis, 1954). See also MGI.

Ph, patch, semidominant, XVII, Chapter 21. Arose spontaneously in the C57BL strain. Heterozygotes have sharply defined white spotting in the belt region. The spot may vary from a large belly spot to a wide complete belt which includes the fore and hind legs. The skull is a little wider and shorter than normal and has a large interfrontal bone. Homozygotes die in utero from about 10 days of gestation onward. At 9 days they have an excessive amount of fluid in the circulation, the pericardium, the tissues, and under the epidermis. Those that survive the 10-day period have a large bleb in the middle of the face which interferes with the development of the nose and palate ( Grüneberg and Truslove, 1960). See also MGI.

pi, pirouette, recessive, XVII, Chapter 32. Found by Woolley and Dickie ( 1945) as a spontaneous mutation in the C3H strain. Somewhat less viable and fertile than normal. Males are more reliable breeders than females. Homozygotes show the typical behavior of the circling mutants, circling, head-tossing, hyperactivity, and deafness. Deafness may be present from the beginning or may be delayed until 1 to 4 months of age depending on the genetic background ( Kocher, 1960a). Behavioral abnormalities are due to degenerative changes in the inner ear including degeneration of Corti's organ, the spiral ganglion, stria vascularis, saccular maccula, and (after 9 months) the cristae ampullaris ( Deol, 1956b; Kocher, 1960a). See also MGI.

pk, plucked, recessive, linkage not known. Arose in the DBA/2J strain. Not allelic with ic or hr. Homozygotes develop a thickened folded skin with no fur at 5 days of age when normal mice have begun to show their first coat. The skin gradually becomes thinner and by 30 days areas of very short fur have developed. The tail lacks fur. Both sexes are fertile ( Dickie, 1965). See also MGI.

pl, platino, recessive, linkage not known. Arose in the C57BL/10- H-2^d strain. Homozygotes are near white with dark eyes. They resemble c^e/ c^e but pl is not allelic with c^e. Tests with other loci have not been reported. Homozygotes are fully viable ( Pizarro, 1957). See also MGI.

pn, pugnose, recessive, III. Arose spontaneously in the S strain at the Rockefeller Institute for Medical Research. Homozygotes are distinguishable at 4 weeks by the relatively shorter, wider head. The forehead protrudes slightly and the skin over the nose is wrinkled. Adults are 2 to 4 g lighter than their normal littermates. The parietal, frontal, and nasal bones and the mandible are shorter and wider than normal. The xiphisternum is bent ventrally. There is reduced survival to weaning. Males are normally fertile but females are poor breeders, often failing to deliver their young or care for them properly ( Kidwell et al., 1961). See also MGI.

Po, postaxial polydactyly, dominant, linkage not known, Chapter 15. Found in mice obtained from a fancier in Japan. This abnormality is characterized by an extra toe on the ulnar side of one or both forefeet. The character depends on a major dominant gene ( Po) and possibly some minor genes which may modify its expression ( Nakamura et al., 1963). See also MGI.

Pre locus, prealbumin component, linkage not known, Chapter 15. Two alleles are known at this locus: Pre^a, presence of a minor prealbumin component of serum protein, detected by starch-gel electrophoresis and found in the AKR/J, BALB/cJ, CBA/J and other strains; and Pre⁰, absence of this component found in the A/HeJ, C57BL/6J and other strains. The function of the prealbumin component is not known ( Shreffler 1964a). See also MGI.

Ps, polysyndactyly, semidominant, linkage not known. Arose in a low-intensity neutron irradiation experiment. In heterozygotes forefeet show postaxial poly- and syndactyly, as well as preaxial fragmentation of the pollex. In hind feet the hallux is shortened and thickened; other digits may be shortened or syndactylous. Homozygotes die shortly after birth with malformed feet in which all digits seem to be syndactylous. Claws are vestigial in heterozygotes and absent in homozygotes ( Searle, 1965). See also MGI.

Pt, pintail, semidominant, VIII. Arose in a strain protractedly treated with methylcholanthrene. Heterozygotes have tails of variable length usually characterized by kinks near the end and a thin threadlike tip. Homozygotes have tails similar to those of heterozygotes but usually much shorter. Homozygotes are smaller than normal and have a high preweaning mortality rate, but survivors are healthy and fertile ( Hollander and Strong, 1951). Examination of the skeletons of Pt/+ and Pt/Pt mice shows that there is a progressive reduction of the nucleus pulposus of the intervertebral discs in a cephalocaudad direction. The reduction is more severe in Pt/Pt than in Pt/+. The defect can be traced back to the 10th day of embryonic development where it appears as a reduced rate of cell division of the notochord. This leads to a smaller than normal notochord, and this in turn to small intervertebral discs (Berry, 1960, 1961b). See also MGI.

ptr, pulmonary tumor resistance, recessive, linkage not known. The C57BL/Fa and A/Fa inbred strains differ at a single locus with large effect on resistance to urethane-induced lung tumors. The allele in C57BL/Fa, ptr, acts as a recessive and appears also to be recessive to the alleles in several other inbred strains ( Bloom and Falconer, 1964). See also MGI.

pu, pudgy, recessive, I, 8-2E. Appeared in descendants of an X-rayed male. Homozygotes are identifiable at birth by their extremely short tails and shortened trunk region. The whole vertebral column is greatly shortened and highly irregular. Ribs and sternum are also abnormal. The rest of the skeleton is normal. Viability is somewhat reduced. Females are very poor breeders but many males, surprisingly, breed well. The axial abnormalities arise from defective segmentation. Somite tissue with an epithelially arranged outer layer is formed, but segmentation is abortive or absent ( Grüneberg, 1961b). pu is very possibly and recurrence of stub ( sb). See also MGI.

px, postaxial hemimelia, recessive, XI, Chapter 15. Arose spontaneously in a stock carrying Ra. A similar allele, called px^r, arose at the Oak Ridge National Laboratory. The forelimbs are regularly affected. There may be absence of digits 5, 4, and sometimes 3, and reduction or absence of the ulna. There is always a large, oval foramen in the scapula. The hind limbs are usually normal, but digit 5 may be absent and occasionally the fibula is reduced. On the dorsal surface of both fore and hind feet there are epidermal papillae, situated a little behind the base of the digits, which sometimes develop a rudimentary claw. Mice with more severely affected limbs tend to have an extra pair of ribs and a slight reduction in number of presacral vertebrae. Both sexes are sterile and show abnormalities of the Müllerian ducts including a partly or wholly double vagina and uncoiled oviducts in the female, and persistent Müllerian ducts in the male ( Searle, 1964). See also MGI.

py, polydactyly, XIII, Chapter 15. Polydactyly unassociated with other major defects has been described several times in the mouse. In one such case, described by Holt ( 1945), the polydactyly is on the preaxial side and affects the hind feet almost exclusively. Penetrance is variable and may be increased by selection. In appropriate stocks it has been possible to follow the segregation of this gene sufficiently to determine its linkage ( Fisher, 1953). In stocks selected for regular manifestation of py/py, heterozygotes ( py/+) were occasionally polydactylous on one foot ( Parsons, 1958a). py is therefore not completely recessive. See also MGI.

Q, quinky, semidominant, linkage not known. Like Kw but not tested for allelism with it. Not linked to T. Arose as a spontaneous mutation in the Q strain. Heterozygotes are viable and fertile, but penetrance is incomplete. Heterozygotes may have short kinked tails and shaking or circling behavior. Most homozygotes die soon after implantation ( Schaible, 1961). See also MGI.

qk, quaking, recessive, linkage not known, Chapter 32. Arose spontaneously in the DBA/2J strain. Homozygotes have a marked rapid tremor which disappears when the mouse is at rest and in contact with bedding, but increases during locomotion. The tremor is most marked in the caudal part of the trunk. It begins at about 10 to 12 days and is fully developed by 3 weeks. Mature mice may have attacks in which a motionless posture is maintained for many seconds. Both sexes are viable and fertile but males seldom sire litters. The entire central nervous system is very deficient in myelin at all ages. Apparently myelin fails to develop. Axons and cells in gray matter appear normal ( Sidman et al., 1964). See also MGI.

qv, quivering, recessive, I. Found as a spontaneous mutation in a noninbred stock ( Yoon and Les, 1957). Viability at weaning is normal but the lifespan is short, the majority dying before 5 months of age. Males are sterile but females may be fertile and nurse their litters. Homozygotes are characterized by locomotor instability, pronounced quivering, varying degrees of paralysis of the hind legs, clasping of the hind legs when held up by the tail, and priapism in most males ( Yoon and Les, 1957; Yoon, 1960). Serial sections of the brain, cord, and nerve roots revealed no abnormalities, and urinary amino acids are normal ( McNutt, 1962). Studies of the effect of qv on serum proteins and serum cholinesterase have been made, but it is not clear how the results are related to the effects of the gene on behavior ( Yoon, 1961a; Yoon and Harris, 1962). See also MGI.

r, rodless retina, recessive, IV, Chapters 29, 32. Found by Keeler ( 1924) in derivatives of the Bagg albino strain. Fully viable and fertile. It may be extinct, although it was found by Keeler ( 1927a) to be widely distributed in various mouse colonies in the United States and to be present in a stock at Berlin-Dahlem. The eyes of homozygotes are devoid of rods and the outer nuclear layer of the retina is reduced. No visual purple is present. The abnormality was not recognized in the first week after birth but was apparent at 13 days ( Keeler, 1927b). Keeler ( 1928) found that rodless mice were blind. See also MGI.

Ra locus, V. See also MGI.

Ra, ragged, semidominant. Arose spontaneously in a crossbred stock. In heterozygotes the first coat develops a little more slowly than normal. The coat contains guard hairs and awls but no auchenes and very few zigzags. This gives the coat a thin, ragged appearance. The agouti pattern is modified in Ra/+, the entire coat being unusually dark. Heterozygotes are normally viable and fertile. Homozygotes are almost completely naked. Many are edematous at birth and most die before weaning. A few survive and may breed ( Carter and Phillips, 1954). Developmental studies have shown that in Ra/+ mice growth of the late-differentiating hair follicles which produce auchenes and zigzags is very retarded or arrested. Growth of nearly all follicles in Ra/Ra mice is arrested ( Slee, 1962). A low percentage of Ra/+ mice in some stocks have a white chylous fluid in the abdomen from shortly after birth until a week or two of age ( Herbertson and Wallace, 1964). The authors have proposed a mutation at a separate closely linked locus as the explanation, but in view of a similar condition in ra^op/+ (see below), it seems more likely that chylous ascites is a pleiotropic effect of Ra. See also MGI.

Ra^op, opossum, semidominant. Appeared spontaneously in a hybrid between the C57BL/6J and DBA/2J inbred strains ( Green and Mann, 1961). Heterozygotes have very sparse fur consisting mostly of guard hairs and awls. The anterior vibrissae are absent. Viability is low, many heterozygotes dying shortly after birth in an edematous condition. Some develop a white fluid in the peritoneal cavity as in Ra/+ and usually die before weaning. The surviving females are very poor breeders, but males may be normally fertile. Homozygotes die in utero, probably before 11 days. Ra/Ra^op mice also die in utero, probably before 11 days ( Mann, 1963). See also MGI.

rd, retinal degeneration, recessive, XVII, Chapters 29, 32. Described by Brückner ( 1951) and Tansley ( 1954) in various stocks and later found to be present in many inbred strains including C3H/He, C3H/St, C3H/Ha, C3HeB/Fe, P/J, BDP/J, PL/J, ST/J, SJL/J, and CBA/J. Homozygotes are fully viable and fertile. Eyes develop normally up to about the 12th day of age. At this stage the outer segment of the rod cell has begun to form, and in normal mice it elongates rapidly during the 12th and 13th day. In rd/rd mice the outer segments which have begun to form, degenerate during the 12th and 13th day. The rod cells degenerate and by the 21st day have disappeared ( Sidman, 1961). See also MGI.

Re, rex, dominant, VII. First described by Crew and Auerbach ( 1939) who obtained it from a commercial breeder. Both homozygotes and heterozygotes are fully viable and fertile. Homozygotes have a slightly more extreme expression than heterozygotes when young ( Carter, 1951b). Both have curly whiskers and wavy coats. The waviness of the coat disappears in adults but the vibrissae and guard hairs remain curly. See also MGI.

Rf, rib fusion, semidominant, linkage not known. Arose spontaneously in strain 129/RrSv. Heterozygotes have various skeletal anomalies, the commonest of which is the fusion of ribs, usually somewhat distal to the vertebrae. The vertebrae may also be abnormal, and the tail may be kinked. Homozygotes have very abnormal shortened vertebral columns and a short wide thoracic basket with extensive neural arch and rib fusions ( Mackensen and Stevens, 1960). Embryos of homozygotes fail to form somites. The rib fusions of heterozygotes are probably the result of abnormalities of the ventrolateral extensions of otherwise normal somites ( Theiler and Stevens, 1960). See also MGI.

rl, reeler, recessive, XVII, Chapter 32. Found by Falconer ( 1951) as a spontaneous mutation in a mildly inbred stock. Homozygotes are unable to keep their hindquarters upright and frequently fall over on their sides when walking or running. Viability is much reduced. Males are sterile and females almost always so. Falconer thought that reelers appeared mentally deficient. Subsequent investigation showed that in reelers the typical organization and lamination of the cerebellar cortex, the cerebral cortex, and the hippocampal cortex are destroyed ( Hamburgh, 1963; Meier and Hoag, 1962). The cerebellum is much smaller than normal, but the cholinesterase activity per unit of wet weight is about twice that of normal ( Hamburgh, 1963). See also MGI.

ro, rough, recessive, V. Arose spontaneously in the RIII inbred strain. Homozygotes have wavy vibrissae, apparent a few days after birth and still visible, though reduced, in the adult. The hair of the coat is not wavy, but the hairs tend to stick together in bundles as if wet or greasy. The septa between the air spaces of the hair are thicker and the air spaces smaller than normal. Many of the air spaces are filled with fluid which does not dry out because the hairs are greasier than normal ( Falconer and Snell, 1952). See also MGI.

Rp, reduced pinna, semidominant, linkage not known. Occurred spontaneously in a randombred stock. Heterozygotes have either or both pinnae affected. Expression varies from a slight reduction along the dorsal edge of one pinna to an almost complete absence of the pinna. Homozygotes do not live past 9 days of gestation. Up to this stage abnormal embryos may be recognized by inversion of the head or tail folds of the ectoderm so that all or part of the embryo lies outside of the yolk sac. Penetrance in heterozygotes is incomplete and can be improved by selection ( Lyon and Meredith, 1963).

ru, ruby-eye, recessive, XII, Chapter 21. Found by Dunn ( 1945) in a silver piebald stock of Danforth. Homozygotes at birth have unpigmented eyes which later darken to a dark ruby color. The black pigment of the coat is diluted to a dark slate color, and the yellow pigment is diluted slightly. Ruby in homozygous condition has the same effect on shape of the pigment granules as b, i.e., it makes them spheroidal rather than ovoid as in wild type, and it changes the color of the granules to dark brown. It greatly reduces the number of melanocytes in the retina, ear skin, Harderian gland, and nictitans ( Markert and Silvers, 1956). See also MGI.

Rw, rump white, semidominant, linkage not known. Arose in a low-intensity neutron irradiation experiment. Heterozygotes show partial depigmentation confined to the posterior end of the body. The tail, hind legs, and area around the base of the tail are usually white. The white area is more extensive ventrally than dorsally. Homozygotes probably die before birth ( Searle, 1965). See also MGI.

s locus, III, Chapters 15, 21, 29. Radiation-induced mutation at this locus is very common ( W.L. Russell, 1965). See also MGI.

s, piebald, recessive. This is a very old mutant and it is possible that some piebalds in existing stocks may be of independent origin. Homozygotes show irregular white spotting, the amount of which is greatly influenced by minor modifying genes ( Dunn and Charles, 1937). They have dark eyes. The white areas are completely lacking in melanocytes in the choroid layer of the eye ( Markert and Silvers, 1956; Billingham and Silvers, 1960). There may also be defects in the structure of the iris, suggesting that pigment cells make some structural or inductive contribution to normal development of the iris ( Dunn and Mohr, 1952). Homozygotes may develop megacolon which is always associated with lack of ganglion cells in the distal portion of the colon. The incidence of megacolon is affected by minor modifying genes ( Bielschowsky and Schofield, 1962). Mayer ( 1965) has shown by explantation of embryonic tissues that the defect leading to white spotting is in the neural crest rather than in the skin. See also MGI.

s^l, piebald-lethal. Found in the F₂ of a cross between C3H/HeJ and C57BL/6J. This allele is recessive to wild type and nearly recessive to s. Homozygotes are almost completely white with dark eyes and with only an occasional small pigmented spot on the head or rump ( Lane, 1962a). All homozygotes develop megacolon with lack of ganglion cells in the posterior end of the colon. They usually die at about 2 weeks of age, but some live for a year or more and may breed ( Lane, 1966). See also MGI.

sa, satin, recessive, XIV. Possibly radiation-induced. Homozygotes are viable and fertile. The hair texture is altered to produce a silky coat with a high sheen. The effect is probably on the cellular arrangement within each type of hair rather than changes in distribution of different types of hair ( Major, 1955). See also MGI.

sb, stub, recessive, linkage not known. This mutant is extinct but may possibly have recurred in pu which it resembles closely. It arose in the inbred CF #1 stock of Carworth Farms. The embryology of sb was not studied, but the description of postnatal homozygotes differs in no way from that of pu ( Dunn and Gluecksohn-Schoenheimer, 1942). See also MGI.

sc, screw-tail, recessive, linkage not known, extinct, Chapter 15. Arose spontaneously in the inbred Bagg albino strain at Cold Spring Harbor. Homozygotes show widespread abnormalities of the skeleton including shortened kinked tails, defective vertebral centra which may result in sharp kinks in the thoracic or lumbar region, a short broad unsegmented sternum, abnormal teeth and jaws, and abnormalities of the calvarium. The number of presacral vertebrae is increased by about one ( MacDowell et al., 1942). The abnormalities of the sternum appear to result from retarded growth of the ribs which fails to bring the bilateral sternal bands into close union ( Bryson, 1945). Abnormalities of dentition appear to result from retarded growth of the mandibular condyle, maxillary sutures, and connective tissue of the dental pulp ( Bhaskar et al., 1951). See also MGI.

Sd, Danforth's short tail, semidominant, V, Chapter 29. Found as a spontaneous mutation by Danforth ( Dunn et al., 1940). Many heterozygotes and all homozygotes die shortly after birth from urogenital abnormalities. The surviving heterozygotes may have good viability and fertility. Heterozygotes have short tails with a reduced number of caudal vertebrae and some kinking. Tails may be absent and the third and fourth sacral vertebrae missing. The bodies of all the vertebrae are reduced ( Grüneberg, 1953a). One or both kidneys may be reduced in size or absent. In the absence of kidney its ureter may be short or absent. Homozygotes have similar but much more severe abnormalities. In addition the anus is imperforate and the rectum and sometimes the urethra and bladder are absent ( Gluecksohn-Schoenheimer, 1943). The developmental effects can be traced to a structurally abnormal notochord, more severe toward the caudal end, leading to abnormal vertebrae and to reduction of the cloaca and tail gut ( Grüneberg, 1958a). Organ-culture experiments attempting to determine whether the lack of kidneys in Sd/Sd embryos is due to defective kidney mesenchyme or to defective ureters indicated that both are quantitatively defective ( Gluecksohn-Waelsch and Rota, 1963; Chapter 25). See also MGI.

se, short-ear, recessive, II, Chapter 29. Arose spontaneously in mice obtained from a commercial breeder ( Lynch, 1921). Homozygotes have short, slightly ruffled ears recognizable at about 14 days of age. The defective ears are due to a defective cartilage framework. The whole skeleton is abnormal, being slightly smaller than normal with numerous local defects including a reduced or bifurcated xiphisternum, reduced number of ribs and sternebrae, reduction or absence of the ulnar sesamoid bone of the wrist, the medial sesamoid bone of the knee, and the anterior tubercules of the sixth cervical vertebra, and other similar defects ( Green, 1951). The skeletal abnormalities are traceable to defective condensation of mesenchyme in the embryo ( Green and Green, 1942). In the adult, proliferation of periosteal cells in the healing of bone fractures is reduced in se/se mice ( Green, 1958). Homozygotes also show variable frequency of abnormalities of the soft tissues probably secondary to the skeletal defects and including hydroureter and hydronephrosis, multiple lung cysts, medially displaced left ovary, displaced right renal artery, and multiple small giant cell granulomas on the ventral surface of the liver (Green, unpublished). Viability and fertility of homozygotes are normal on some genetic backgrounds but reduced on others. See also MGI.

sf, scurfy, recessive, XX (sex-linked). Arose spontaneously. Hemizygous males can first be recognized at about 11 days of age by a reddening of the genital papilla. They develop scaliness, first of the tail and later of other parts of the body. The skin appears tight, and the eyelids open late. Scurfy males usually die before or shortly after weaning. The survivors are small and sterile. Occasional scurfy females have occurred and have proven to be X/O in sex chromosome type. These females resemble scurfy males in appearance and viability ( W.L. Russell et al., 1959). See also MGI.

sg, staggerer, recessive, II. Occurred spontaneously in a stock of obese mice in 1955. Homozygotes usually die during the fourth week. Some survive to adulthood, and one male has bred. Homozygotes show a staggering gait, mild tremor, hypotonia, and small size. The cerebellar cortex is grossly underdeveloped with too few granule cells and unaligned Purkinje cells ( Sidman et al., 1962). See also MGI.

sh-1, shaker-1, recessive, I, Chapter 32. Found by Lord and Gates ( 1929) in a Bagg albino strain. Viability is normal and breeding ability is high for a circling mutant. Homozygotes show the circling, head-tossing, deafness, and hyperactivity characteristic of mutants of this type. They can sometimes hear and swim well on the surface of water up to 4 weeks or more but lose the ability later. The degenerative changes of the labyrinth may occur a little late than in some of the other waltzing mutants. They consist of degeneration of the organ or Corti, the spiral ganglion, and the stria vascularis in the cochlea, and of the saccular macula and the vestibular ganglion in the vestibular labyrinth ( Deol, 1956b). The eighth nerve action potential and the cochlear potentials begin to develop but are never normal and have disappeared by 22 days of age ( Mikaelian and Ruben, 1964). The double heterozygote, sh-1/+ v/+ becomes deaf at 10 weeks to 8 months with some degeneration in the organ of Corti. See also MGI.

sh-2, shaker-2, recessive, VII, Chapter 32. Discovered by Dobrovolskaïa-Zavadskaïa ( 1928) in the descendants of an irradiated male. Viability and fertility are nearly normal. This mutant is very similar in behavior and pathology to sh-1, with the exception that the abnormalities are observed a little earlier in sh-2. Homozygotes appear to be deaf from the beginning, and the saccular macula is abnormal at birth ( Deol, 1954). See also MGI.

Sha, shaven, semidominant, VI. Arose in stock of the Endocrinology Department, Edinburgh. Heterozygotes have curled whiskers and a "greasy" coat. Homozygotes grow sparse coats of very short hair. The histology of homozygotes is very much like that of N, to which Sha is closely linked ( Isaacson and Cattanach, 1962; Falconer and Flanagan, 1963). See also MGI.

sho, shorthead, recessive, linkage not known, Chapter 15. Arose spontaneously in an inbred line at the Nevis Biological Station of Columbia University. Newborn homozygotes are characterized by small size, disproportionate shortening of the head and limbs, and a large median cleft palate. They die soon after birth. The forelimbs are relatively more shortened than the hind limbs. The small intestine is about one-half normal length, and in females one ovary or oviduct may occur medial to the kidney on that side. At 14 days of gestation the chondrocranium is severely foreshortened and the part of the basal plate that will become the preshenoid is widened. Mutants can be recognized at 12 days of gestation by their small size and short heads, showing that the gene acts before cartilage formation ( Fitch, 1961a). The cleft palate can be traced to 14-day embryos, when the tongue and lower jaw are seen to be abnormally small and the palatal shelves are prematurely closed at their anterior end. They enclose the tip of the tongue preventing it from descending and thereby preventing the posterior part of the shelves from closing ( Fitch, 1961b). See also MGI.

si, silver, recessive, IV, Chapter 21. This mutant is widespread in the English fancy. Homozygotes are extremely variable in appearance. Individual hairs of the coat of nonagouti silvers may be all white, all black, black with white tips, or white with gray or black bands. Silvering results from a reduction in number of pigment granules. Nonagouti silvers heterozygous for brown (si/si a/ a b/+) have very light underfur ( Dunn and Thigpen, 1930). The effect of si is so variable that it is often difficult to classify in crosses, and its usefulness as a genetic marker is therefore limited. See also MGI.

Sk, scaly, semidominant, linkage not known. Arose spontaneously. Penetrance is probably complete in heterozygotes. In mild cases they show scaliness on shoulders and back of head only; in extreme expression the scaliness may cover the entire dorsal surface and ears, producing almost immobile animals which occasionally die. Scaliness is first noticeable at about 4 days. The coat grows in sparsely at first but may in milder cases become indistinguishable from normal. The fate of the homozygotes is unknown ( Kelly and Bangham, 1955). See also MGI.

Sl locus, IV, Chapters 15, 17, 21, 29. Mutants at this locus are very common and have occurred in many laboratories. See also MGI.

Sl, steel, semidominant. Arose spontaneously in the C3H inbred strain ( Sarvella and Russell, 1956). Heterozygotes have a slight dilution of the coat color, more extreme on the belly than on the back, light ears, feet, and tail, and occasionally a belly spot or blaze. They also have a slight macrocytic anemia but are viable and fertile. Homozygotes are severely anemic in utero and die usually at 15 to 16 days of gestation ( Sarvella and Russell, 1956). Primitive germ cells are absent in Sl/Sl and deficient in Sl/+. There is no pigment forming ability in the skin of Sl/Sl embryos ( Bennett, 1956). See also MGI.

Sl^d, steel-Dickie, semidominant. Arose spontaneously in the DBA/2J inbred strain ( Bernstein, 1960). This allele is similar to Sl in its effect on coat color in heterozygotes, but homozygotes are viable. They are white with black eyes, severely anemic, and sterile. Sl/Sl^d mice are also black-eyed white and anemic and many live as long as a year. Both Sl^d/Sl^d and Sl/Sl^d are sterile with very few germ cells in the gonads. The germ-cell-deficient ovaries develop tumors in old age (Bernstein and Russell, 1965, personal communication). See also MGI.

Sl^gb, grizzle-belly, semidominant. Arose spontaneously in a belted white female. Heterozygotes have light bellies. Homozygotes are anemic and die during the first week of life (Schaible, 1961, 1963b). See also MGI.

Sl^so, sooty, semidominant. Arose in the C57BL/6 strain. Sl^so/+ mice have a dilute coat and light tail. Sl^so/Sl^so are black-eyed white and anemic but live 10 to 40 days ( Miller, 1963; Hollander, 1964). See also MGI.

sla, sex-linked anemia, XX (sex-linked), Chapter 17. Probably radiation-induced. There is some misclassification. Two heterozygous females were classified as anemic, so it is uncertain whether sla is completely recessive ( Falconer and Isaacson, 1962a). Homozygous females and hemizygous males can be recognized at birth by their pale color and small size. The color becomes normal within a few days, but the size difference persists throughout life. An abnormal blood picture persists virtually unchanged throughout life and consists in a red cell count about three-quarters of normal and a slight reduction in mean corpuscular hemoglobin concentration and cell size. There is reduction of hemopoietic tissue in both liver and bone marrow ( Grewal, 1962b). See also MGI.

sm, syndactylism, recessive, linkage not known, Chapter 15. Arose spontaneously in the A/Fa inbred strain ( Grüneberg, 1956). There is considerable preweaning mortality of homozygotes. Fertility is about normal in surviving males but low in females. Homozygotes have all four feet affected. The third and fourth digits are always syndactylous and the first and second sometimes so. Digits of the forefeet are usually joined by soft tissue only, digits of the hind feet by fusions of cartilage and bone. Many homozygotes have tail kinks. The defect can be traced to hyperplasia of the apical ectodermal ridge of the limbs, of part of the limb epidermis, and of the epidermis in the distal part of the tail. Enlargement and deformation of the foot plates follows. The foot plates are bent over in a palmar direction causing crowding of the middle digits. The enlargement of the foot plates is thought to result from increased stimulation of mesenchymal growth by the hyperplastic ectodermal ridge ( Grüneberg, 1960). See also MGI.

sn, scanty, recessive, linkage not known. Found in offspring of a cross. Homozygotes grow a thin coat of uneven hair. The thickness of the coat is variable in an individual and between individuals. The coat starts thinning out after some months, but this process also is variable. By 9 months the coat is usually very ragged, consisting of small tufts of hair. Homozygotes are usually small and difficult to breed ( Nolte, 1957).

So, sombre, semidominant, XVIII. Arose spontaneously in the C3H inbred strain ( Bateman, 1961). Heterozygotes resemble nonagouti ( a/ a) except that they have a stronger tendency to develop yellow hairs on their sides as they mature. Homozygotes are black all over. Except for a few yellowed hairs on the perineum they exactly resemble extreme nonagoutis ( a^e/ a^e). Viability and fertility are normal in both homozygotes and heterozygotes. See also MGI.

Sp locus, XIII, Chapter 21. Mutations at this locus occur frequently ( Dickie, 1964a). See also MGI.

Sp, splotch, semidominant. Arose spontaneously in the C57BL inbred strain ( W.L. Russell, 1947). Heterozygotes show white spotting on the belly and occasionally on the back, feet, and tail. Homozygotes die at 13 days of gestation with malformations which include rachischisis in the lumbosacral region and frequently in the region of the hindbrain, overgrowth of the neural tissue, reduction or absence of spinal ganglia and their derivatives, and abnormal tail morphology. Neural crest and the adjacent regions of Sp/Sp embryos fail to develop any pigment when transplanted to chick coelom or to the anterior chamber of mouse eyes ( Auerbach, 1954). See also MGI.

Sp^d, delayed splotch, semidominant. Arose spontaneously in the C57BL/6J strain. Heterozygotes have a white belly spot. Homozygotes are similar to Sp/ Sp but have caudal rachischisis only, and survive to birth. Sp^d/ Sp mice resemble Sp^d/Sp^d ( Dickie, 1964a). See also MGI.

spa, spastic, recessive, linkage not known, Figure 8-2G, Chapters 23, 32. Found in a hybrid stock by Chai ( 1961). Preweaning mortality is high and breeding performance is low. Homozygotes can usually be recognized at 14 days of age but sometimes not until 5 or 6 weeks. They show spastic symptoms which sometimes occur spontaneously and can always be induced by handling. The spasms consist of rapid tremor, stiffness of posture, and difficulty of righting when placed on the back ( Chai, 1961). The symptoms can be markedly alleviated by intraperitoneal injection of aminooxyacetic acid but not by Dilantin or trimethadione ( Chai et al., 1962). See also MGI.

spf, sparse-fur, recessive, XX (sex-linked). Found in a descendant several generations removed from an irradiated male. In affected mice (presumably homozygous females and hemizygous males) development of the fur is late and patchy. By weaning age the fur looks practically normal ( Cupp, 1958; L.B. Russell, 1960a). See also MGI.

sph, spherocytosis, recessive, linkage not known, Chapter 17. Arose in an unpedigreed C3H stock. Homozygotes are extremely pale at birth and acquire a yellow color during the first few hours thereafter. They die within the first 24 hours. Examination of the blood shows numerous spherocytes accompanied by all the evidence of hemolytic anemia ( Joe et al., 1962). See also MGI.

sr, spinner, recessive, linkage not known. Arose spontaneously in the C57BL/How inbred strain. Homozygotes show the typical head-tossing, circling, deafness, and hyperactivity of the shaker-waltzer mutants. The abnormal behavior can be recognized as early as 7 days. The anomalies of the inner ear consist of degeneration of the organ of Corti and spiral ganglion and reduction in size of the stria vascularis of the cochlea, and of lesser degeneration of the vestibular part of the labyrinth limited to the saccular macula. Both sexes are fertile but females do not make good mothers ( Deol and Robins, 1962). See also MGI.

Ss locus, serum serological, semidominant, IX, Chapter 24. Two alleles are known which differ in the amount of a serologically detected serum globulin. Ss^h determines a high level of the component and Ss^l determines a low level. No qualitative difference has been found between the proteins determined by the two alleles. The Ss locus is either very closely linked to H-2 or identical with it. Ss^l has been found in all H-2^k strains and Ss^h in all other strains examined ( Shreffler and Owen, 1963; Shreffler, 1964b). See also MGI.

st, shaker-short, recessive, linkage not known. Probably extinct. Arose in a stock of hairless mice ( Dunn, 1934). Viability is much reduced. Females were sterile but a few males bred. Most newborn homozygotes have one or two cerebral hernias covered by skin near the median point of the parieto-occipital suture of the skull. The blebs later dry to a scab. Tail length varies from absence to three-quarters normal length. From 5 days on there is disturbed equilibrium with erratic circus movements and in adults marked lack of coordination. In the development of the brain no foramen of Magendie or choroid plexus is formed, leading to disturbed circulation of the cerebrospinal fluid ( Bonnevie, 1936). By the 16th day of gestation the lumen of the brain is narrow and the walls are abnormally thick. About the 17th day there is a rupture of the roof of the mesencephalon and cerebellum, which gives rise to the cerebral hernias. The ear vesicles, as in kreisler, are very abnormal in morphology, possibly because of a separation of the vesicles from the inductive influence of the myelencephalon. See also MGI.

stb, stubby, recessive, V. Found in a linkage cross. Resembles achondroplasia ( cn) but is less severe. Homozygotes are recognizable shortly after birth by the stubby appearance of the head. Adults have shorter heads, bodies, and legs than normal but there is some variation in expression. Most females are fertile and bring up their litters but males are probably sterile ( Lane, 1965). See also MGI.

Str, striated, semidominant, XX (sex-linked), Chapter 15. Found among the progeny of an X-rayed male. Heterozygous females show a transverse striping similar to Ta/+ females. The dark stripes are due to shortening of the hairs and not to a lack of zigzags as in Ta/+. Viability appears to be normal, but there is a shortage of Str/+ in segregating generations probably due to misclassification. Hemizygous males die at about 11 to 13 days of gestation ( Phillips, 1963b). See also MGI.

su, surdescens, recessive, linkage not known. Found in mice of the C57BL/Gr inbred strain and in a strain carrying Mi^wh ( Kocher, 1960b). Homozygotes hear normally when young but become deaf or hard of hearing between 2 and 5 months. Behavior is normal. In some su/su mice reduction in size of the stria vascularis and degeneration of the organ of Corti and the spiral ganglion are found. In others the changes are more severe and include also a decrease in the size of the endolymphatic space in the scala media and the sacculus, somewhat resembling the changes caused by sy. Middle ear abnormalities also occur in su/su ( Kocher, 1960b). See also MGI.

sv, Snell's waltzer, recessive, II. Found in a histocompatibility stock of Snell ( Green, 1960). Viability is nearly normal. Breeding ability is reduced, and males are more reliable breeders than females. Homozygotes show the typical circling, head-tossing, deafness, and hyperactivity of other mutants of this type. They have defects of the membranous labyrinth similar to those of Va, with degeneration occurring in the cristae as well as in other parts of the labyrinth (Deol, 1965, personal communication). See also MGI.

sy, shaker with syndactylism, recessive, linkage not known, Chapter 15. Found by Hertwig ( 1942) among the descendants of an irradiated male. Most homozygotes die within the first month and none have lived to breed. Homozygotes may be syndactylous on all four feet; the forefeet may often be normal and possibly one or both hind feet very occasionally so. The remainder of the skeleton shows many slight anomalies in addition to small size. The shafts of the long bones are considerably thinner than normal, and there are differences in shape of the sacral vertebrae and the scapula ( Grüneberg, 1956). The osseous skeleton is less densely constructed than normal ( Grüneberg, 1962). Abnormal behavior appears during the first week. It consists of head-tossing and some circling, and the affected mice are always deaf. Abnormalities of the labyrinth can be seen at 13 days of gestation. There is an excessive amount of mesenchymal tissue from which develops an excessive amount of perilymphatic space. Partial collapse of the endolymphatic space follows and eventually extensive degeneration of all parts of the membranous labyrinth occurs. A quantitative abnormality of the mesodermal tissue has been suggested as the basis of the whole syndrome ( Deol, 1963). See also MGI.

T locus, IX. At this very complex locus several semidominant ( T) and numerous recessive ( tⁿ) alleles are known. In general T/+ mice are short tailed, tⁿ/+ mice are normal, T/ tⁿ mice are tailless ( Figure 8-2D) and the T/ T and tⁿ/ tⁿ homozygotes are lethal. For some t alleles homozygotes are viable and normal tailed. Compounds of two different alleles (tⁿ/t^m) are usually normal tailed and viable but males are sterile. The t alleles greatly reduce crossing over in this region of linkage group IX and are thus probably chromosome abnormalities of some kind. They mutate frequently to new t alleles and such mutations are usually accompanied by crossing over ( Lyon and Phillips, 1959). Lyon and Meredith ( 1964), after examining the properties of a number of t alleles, have concluded that they probably consist of a functional change in chromatin covering various lengths of chromosome between T and tf and perhaps beyond. Loss of specific pairing might cause unequal crossing over which gives rise to small duplications or deficiencies, thus producing new alleles.

The segregation ratios in males but not in females of the genotype tⁿ/+ or T/ tⁿ are very abnormal, usually with a large excess of offspring from the t-bearing gametes. In wild populations and probably also in some laboratory populations t alleles may be very common. Once introduced they are maintained by their high segregation ratios in spite of the lethality of the homozygotes (see Grüneberg, 1952, chapter XV; Dunn et al. 1960, 1962 for a more complete description and references). The sperm and spermatogenesis of T/ tⁿ and tⁿ/+ males appear normal, but the t-bearing sperm fertilize a disproportionately high number of eggs when such males are mated. The proportion becomes more nearly normal if matings are made late in the estrous period of the female so that a shorter interval occurs between ejaculation and fertilization ( Yanagisawa et al., 1961). On the other hand, the sterile males that are compounds of two lethal t alleles or of a lethal and a viable t produce sperm of normal numbers and appearance but unable to effect fertilization ( Braden and Gluecksohn-Waelsch, 1958). No mechanism has yet been proposed to account for both of these effects. Some of the alleles and their effects are:

See also MGI.

T, brachyury, Chapter 15. Discovered by Dobrovolskaïa-Zavadskaïa ( 1927). Tail length of heterozygotes varies from nearly normal to absent. A few or nearly all tail vertebrae may be missing. There tends to be one fewer presacral vertebra than in +/+ sibs. Studies of development have shown that the notochord in the tail region is abnormal ( Chesley, 1935). Grüneberg ( 1958b) later showed that the notochord was present in the whole tail but tended to become incorporated either in the neural tube or the tail gut. T/T embryos never develop a notochord or only a rudimentary one, the neural tube and somites are irregular, and the posterior portion of the body is greatly reduced. They die at 10 days of gestation ( Chesley, 1935). In organ culture, T/T neural tube can induce cartilage in normal somites, but cartilage cannot be induced in T/T somites ( Bennett, 1958; Chapter 25). See also MGI.

T^H, T-Harwell. Found in the control series of an irradiation experiment. T^H/+ are indistinguishable for T/+ but T^H/T^H die at an earlier stage than T/ T, being already highly abnormal at 8 days ( Lyon, 1959). See also MGI.

t⁰ - tⁿ, tailless-0 to tailless-n, t^w1 - t^wn tailless wild-1 to tailless wild-n. See Dunn et al. ( 1962) for review of the genetics, and Bennett et al. ( 1959) for description of the effects in homozygotes and compounds. Briefly, tⁿ/tⁿ or t^wn/t^wn mice are either normal, or die at a very early stage with abnormalities which are primarily ectodermal, or die at a late fetal stage with striking pycnosis and degeneration of the ventral portion of the neural tube. See also MGI.

t^b, tailless-b ( Braden and Gluecksohn-Waelsch, 1958).

t^e, tailless-Edinburgh ( Bateman, 1960). See also Mouse News Letter for unpublished alleles.

Ta locus, XX (sex-linked), Chapters 14, 15. See also MGI.

Ta, Tabby, semidominant. Arose spontaneously in a strain selected for large size ( Falconer, 1953). Hemizygous males and homozygous females are identical in phenotype with homozygous crinkled mice ( cr/ cr). They are characterized by absence of guard hairs in the coat, a bald patch behind each ear, bald tail with a few kinks near the tip, reduced aperture of the eyelids, a respiratory disorder, and a modified agouti pattern. Heterozygous females are most easily recognized if they are agouti, in which case they show transverse dark stripes. The dark stripes have no agouti bands on the hairs. Guard hairs are present in the bands, but zigzags are very deficient or absent. Tabby males breed satisfactorily but homozygous females are often sterile. Heterozygous females are fully fertile ( Falconer, 1953). See also MGI.

Ta^J, Tabby-J, semidominant. Arose spontaneously in the 129/Sv inbred strain. Ta^J resembles Ta except that hemizygous males and homozygous females have some hair on the tails, and the hairs are curved. Ta/Ta^J females have both hairless areas and areas with curved hairs on their tails ( Stevens, 1963). See also MGI.

tb, tumbler, recessive, linkage not known. Found among offspring of a cross. Homozygotes walk in crab-like fashion. They may somersault, fall over, or jump when trying to go forward. They can swim but cannot hold on to a rope. Most homozygotes survive and can breed ( Dickie, 1965). See also MGI.

tc, truncate, recessive, XI. Arose spontaneously in a Swiss albino stock at The Jackson Laboratory ( Theiler, 1957). Penetrance is incomplete. Homozygotes have short or absent tails and many have missing sacral or lumbar vertebrae. In some cases several vertebrae seem to be "picked out" in an intermediate position. The primary effect is an interruption of the notochord at 9½ to 10 days of gestation. The sclerotomic cells, which normally migrate from the somites to the midline under the neural tube to form the vertebrae, degenerate in the region of the interrupted notochord. These defects lead eventually to interruption of the spine, paralysis of the hind legs, difficult parturition in females, and absence of the median ventral fissure of the spinal cord ( Theiler, 1959). See also MGI.

td, torpid, recessive, II. Arose in the DBA/2J strain. Homozygotes move very slowly. They may lie on their backs for minutes at a time, sometimes with the mouth and feet quivering. When standing one foot often is raised and quivers. Homozygotes are viable. Both sexes are fertile, but males are more productive ( Dickie, 1965). See also MGI.

tf, tufted, recessive, IX. Probably arose spontaneously in a multiple recessive stock. Homozygotes show repeated waves of hair loss and regrowth which begin at the nose and pass posteriorly along the body. Viability and penetrance are good ( Lyon, 1956). See also MGI.

tg, tottering, recessive, XVIII, Chapter 32. Found in the DBA/2J strain as a spontaneous mutant ( Green and Sidman, 1962). Viability is nearly normal. Homozygotes of both sexes are fertile but breeding performance may be low. Affected mice are characterized by intermittent seizures which may begin as early as 2 weeks of age and continue throughout life, and by a wobbly gait affecting particularly the hindquarters. See also MGI.

th, tilted head, recessive, XIII. Possibly radiation-induced ( Kelly, 1958). Homozygotes are viable and fertile. The head tilts to one side, the side being constant for an individual. The animals shake when held up by the tail. See also MGI.

ti, tipsy, recessive, VII. Found among the descendants of a cross between the C3H/H and 101/H inbred strains. Penetrance is complete and homozygotes are viable and fertile. They have a rabbit-like gait from the age of 1 week., followed soon by a tendency for the forepart of the body to sway from side to side, leading to a reeling locomotion and a tendency to fall over. There is marked variation in expression and some amelioration in older animals ( Searle, 1961). See also MGI.

tk, tail-kinks, recessive, II, Figure 8-2C, Chapter 15. Arose spontaneously in a BALB/c subline at the Chester Beatty Research Institute. Homozygotes are recognized by their shortened kinky tails. The tail vertebrae are very abnormal, and the cervical and upper thoracic vertebrae are also severely affected. There tends to be one more presacral vertebra than normal. The defects can be traced to the 10-day embryonic stage when the cervical sclerotomes in normal mice have differentiated into anterior and posterior halves which differ in density. No such differentiation occurs in tk/tk embryos ( Grüneberg, 1955a). Penetrance is complete and fertility is good. See also MGI.

tl, nonerupted teeth, recessive, linkage not known. Possibly radiation-induced. Homozygotes usually die at weaning but have been raised by special feeding to 3 months. Their teeth do not erupt and there are bony spurs on the long bones and ribs. The tail is slightly shortened ( Kelly, 1955). See also MGI.

Tla locus, thymus leukemia antigen, IX, Chapter 24. This locus determines the presence or absence of an antigen, TL, in the normal thymus. The antigen is present (Tla^a) in thymus of strains A and C58 and absent (Tla^b) in the thymus of strains C57BL/6, C3H/An, BALB/c and AKR ( Old et al., 1963). The antigen is found in no other normal tissue but is found in a proportion of leukemias of probably all mouse strains. Tla^a/Tla^b mice are intermediate between the two homozygotes in the quantity of antigen present in the thymus ( Boyse et al., 1964). Transplantation experiments have shown that the TL type of the thymus cells is determined by their own genotype rather than by the genotype of the thymic stroma or of other cells ( Schlesinger et al., 1965). See also MGI.

tm, tremulous, recessive, linkage not known. Tremor is the most conspicuous symptom of tm/tm mice. They do not have convulsions. Both sexes are sterile. Affected mice have a higher concentration of creatine phosphates and ribose in the supernatant fraction of calcium-precipitated trichloroacetic acid extracts of the brain than their normal sibs ( Yoon and Denuccio, 1963). They also have lower serum cholinesterase and serum β-globulins but higher serum albumin ( Yoon, 1961a; Yoon and Harris, 1962). See also MGI.

tn, teetering, recessive, VII. Arose spontaneously in the C3H/HeJ inbred strain. Homozygotes die between 5 and 6 weeks of age. They are first recognizable at 25 to 30 days by their stiff, slow, unstable movements. They may assume and maintain unusual postures. Just prior to death they look emaciated and lie on their sides with all limbs extended ( Lane, 1962b). See also MGI.

To, tortoiseshell, semidominant, XX (sex-linked), Chapter 21. Arose spontaneously in an obese stock. Heterozygous females resemble Mo/+ females in color. Some have slight skeletal abnormalities of the fore and hind limbs. Hemizygous males die before birth ( Dickie, 1954). To shows about the same linkage relation with Bn as Mo ( Lane, 1960b) and is probably an allele of Mo. See also MGI.

tp, taupe, recessive, I, Chapter 21. Arose spontaneously in the C57BL/10 inbred strain. Viability of homozygotes is normal and fertility of males is normal, but females may have difficulty gestating their young and do not nurse them. Their nipples are abnormal. Homozygotes have a diluted coat color a/ a tp/tp mice being slate gray ( Fielder, 1952). See also MGI.

Tr, trembler, dominant, VII, Chapter 32. Arose as a spontaneous mutation in 1946 in a stock at the Institute of Animal Genetics in Edinburgh ( Falconer, 1951). Mortality of heterozygotes is high at 3 to 4 weeks but can be improved if moist food is provided within easy reach during this critical period. Females breed normally but males are frequently sterile. Homozygotes are viable and cannot be distinguished from heterozygotes. Affected mice show spastic paralysis beginning during the third week, and exhibit convulsions when stimulated. Within a week or two the convulsions usually cease and are replaced by a tremor that consists of very rapid side-to-side movement of the head and neck. The trembling ceases when the mice are at rest. The paralysis persists into adulthood but is less severe ( Falconer, 1951). Tremblers have normal electrocorticograms. Histological examination of the brain and spinal cord has revealed no lesions ( Braverman, 1953). See also MGI.

Trf locus, transferrin, II. Alleles at this locus control variation in the electrophoretic properties of the iron-binding β-globulin component, transferrin, of the serum ( Cohen, 1960; Shreffler, 1960; Cohen and Shreffler, 1961). Ashton and Braden ( 1961). Ashton and Braden ( 1961) and Thompson et al. ( 1954) have independently described variation in the electrophoretic properties of β-globulin which is probably controlled by the Trf locus, although this has not been tested genetically. Two codominant alleles are known, Trf^a, found only in the CBA strain, and Trf^b, found in all other strains tested. The serum component of Trf^a is more negatively charged at pH 8.5 and migrates more rapidly than that of Trf^b. See also MGI.

Ts, tail-short, semidominant, linkage not known, Chapters 15, 17. Arose spontaneously in the BALB/c inbred strain ( Morgan, 1950). Homozygotes probably die before implantation. Viability and expression of heterozygotes is strongly dependent on the genetic background ( Morgan, 1950). Heterozygotes are recognizable by their short kinked tails. They are smaller than normal and have numerous skeletal abnormalities including vertebral fusions and dyssymphyses, bilateral asymmetry of the length of the humerus and the tibia, triphalangy of digit 1 of the forefoot, an additional pair of ribs, and often a shortened and highly abnormal skull. There is a prenatal anemia which disappears before birth and can be traced to a deficiency of the blood islands in the yolk sac of 8-day embryos. The anemia is thought to be the primary effect of Ts and to be the cause of the subsequent abnormalities ( Deol, 1961). See also MGI.

Tw, twirler, semidominant, XV, Chapter 32. Spontaneous. Heterozygotes show head-shaking and circling behavior but are not deaf. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is probably incomplete. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth ( Lyon, 1958). See also MGI.

U, umbrous, semidominant, linkage not known. Found among the descendants of a stock carrying wa-1. U in homozygous condition causes a marked darkening in A/ A mice. In heterozygous condition the darkening is somewhat less. In U/U mice A/ a is distinguishably darker than A/ A. U is thus a modifier of dominance of A ( Mather and North, 1940). No effect of U is recognizable in a/ a mice. A similar mutant has been described by Robinson ( 1959), but no test for allelism have been made. See also MGI.

un, undulated, recessive, V. Found in mice observed from a Cambridge fancier ( Wright, 1947). Homozygotes have a shortened and usually kinked tail. The caudal vertebrae are reduced in size but not in number. The kinks can be flattened out with the fingers but return immediately when released. Some homozygotes have marked kyphosis of the lower thoracic and upper lumbar region. The vertebrae are abnormally formed over the whole spine. The acromion process of the scapula is reduced or absent ( Grüneberg, 1950). The anomalies can be traced to the 11th day of gestation. The condensations of mesenchyme cranial to the sclerotomic fissure are smaller than normal. Instead of joining with the primitive centra in front of them to form the body of the vertebra, they remain with the material posterior to the sclerotomic fissure and enter into the intravertebral disk. The vertebrae are thus smaller than normal and the disks larger than normal ( Grüneberg, 1954b). See also MGI.

Up-1 locus, urinary protein, II. This locus controls variation in the major protein of the urine as revealed by electrophoresis. Two codominant alleles are known: Up-1^a produces the electrophoretic components numbered 1 and 3; Up-1^b produces components 2 and 3. Up-1^a is found in strains BALB/cN, DBA/2Lw, C3H/Lw, NH, C57BR/cd, and some others. Up-1^b is found in C57BL/10Sc, C58, C57L, and some others ( Finlayson et al., 1963). See also MGI.

ur, urogenital, recessive, linkage not known, Chapters 15, 21. Discovered in a balanced tailless stock ( Dunn and Gluecksohn-Schoenheimer, 1947). Homozygotes have short tails and are small at birth. They usually have cleft palates and die within a day or two. Some have normal palates and may survive for a month or more, but they remain small and are sterile. Older animals are usually found to have hydronephrosis or polycystic kidneys. At birth the kidneys have only slight histological abnormalities but are deficient in alkaline phosphatase and probably do not function normally ( Gluecksohn-Waelsch and Kamell, 1955). The skeletal abnormalities consist of a reduction in length but not in width of midline structures, particularly at the anterior and posterior ends. There may be a small extra pair of ribs, and fusions of ribs and sternebrae. The shortening of the skeleton can be seen in the tail at 10½ days of gestation and in the head at 12 days ( Fitch, 1957). The origin of the kidney abnormalities is not known. See also MGI.

uw, underwhite, recessive, linkage not known. Arose spontaneously in the C57BL/6J inbred strain. The fur of homozygotes is a light buff color on top with very white underfur. Eyes are unpigmented at birth but darken to a dark reddish color at maturity ( Dickie, 1964b). See also MGI.

v locus, X, Chapter 32. See also MGI.

v, waltzer, recessive. Probably originated in China many centuries ago ( Keeler, 1931). Viability and breeding ability are somewhat less than normal. Homozygotes show the typical circling, head-tossing, deafness, and hyperactivity of the circling mutants. Most of them are deaf from the beginning. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (v/+ sh-1/+) are deaf beginning at 3 to 6 months. They have changes similar to those of the homozygotes in the organ of Corti, stria vascularis, and spiral ganglion, but less severe and with much later onset ( Deol, 1956b; Kocher, 1960a). See also MGI.

v^df, deaf, recessive. First noticed in a laboratory stock through a somewhat anomalous position of the ears ( Deol, 1956a). Homozygotes may be deaf from the beginning or may hear for a few days before weaning but otherwise behave normally. Deafness is caused by degeneration of the organ of Corti, the spiral ganglion, and the stria vascularis. v/v^df mice are like v^df/v^df mice in hearing ability and behavior. Double heterozygotes with shaker-1 (v^df/+ sh-1/+) become deaf at a late stage ( Kocher, 1960a). See also MGI.

Va, varitint-waddler, semidominant, XVI, Chapter 21, 32. Found by Cloudman and Bunker ( 1945) in descendants of a cross of C57BL x C57BR strains. Viability of heterozygotes is nearly normal but fertility is reduced. Mortality is very high in homozygotes and very few of the survivors are fertile. Heterozygotes are deaf and show circling behavior, head-tossing, and hyperactivity. They circle somewhat less than some of the other circling mutants. Their coats are variegated with patches of normal-colored, diluted, and white fur. Homozygotes show more intense behavioral abnormalities than heterozygotes and their coats are white, except for small patches of unaltered color near the ears and base of the tail ( Cloudman and Bunker, 1945). The pathological changes in heterozygotes include degeneration of the organ of Corti, stria vascularis, spiral ganglion, saccular macula, cristae ampullares, and vestibular ganglion. In homozygotes the degenerative changes are more severe and include also the utricular macula ( Deol, 1954). See also MGI.

vb, vibrator, recessive, probably VII. Arose in the DBA/2J strain. Homozygotes show a constant vibration of the whole body recognizable from about 10 days of age. None live beyond weaning age ( Lane, 1965). See also MGI.

vc, vacillans, recessive, VIII. Arose spontaneously in the DBA/1 inbred strain. Homozygotes can be identified with certainty at 14 days of age by a violent tremor when walking and by swaying of the hindquarters. With age the instability lessens and a ducklike gait sets in. The tremor is less marked with age. Vacillans mice are less aggressive than normal. They are smaller, and females do not take good care of their litters. Muscular strength is about half that of normal mice. There is a peak mortality at weaning age, after which survival appears normal. Sexual maturity in males did not occur before 5½ months. The central nervous system shows no gross anatomical abnormality on pathological examination ( Sirlin, 1956). See also MGI.

Ve, velvet coat, dominant or semidominant, linkage not known. Appeared in offspring of an irradiated male. Heterozygotes closely resemble sa/ sa mice. The coat has a velvety sheen and on the ventral surface appears more luxuriant than normal. Heterozygotes are viable and fertile. The fate of the homozygotes is not known ( Maddux, 1964). See also MGI.

vi, visceral inversion, recessive, linkage not known. Found in descendants of a 4-way cross. Probably extinct. Penetrance is probably not complete, and there may be some loss of homozygotes in segregating generations because of inviability. The mutant resembles iv but was not tested for allelism with it. Homozygotes show complete or partial reversal of the viscera as well as a general sickliness and often hydrocephalus ( Tihen et al., 1948). See also MGI.

vt, vestigial-tail, recessive, VII, Chapter 15. Arose spontaneously in the C57BR inbred strain ( Heston, 1951). Homozygotes have very short tails, varying from complete absence to about half normal length. They tend to have fewer presacral vertebrae than normal, and the bodies of the lumbar vertebrae often ossify from bilateral twin centers rather than from a single center. At 10 days of gestation when there is a ventral ectodermal ridge at the zone of growth of the tail tip, the ridge is much reduced in vt/vt embryos. There is also a reduction in the tail gut. The neural tube in the tail bud is abnormal in the ventral region, tending to split off and round up to form accessory tubes. The abnormality of the ventral ectodermal ridge may be part of the primary effect of the gene ( Grüneberg, 1957). See also MGI.

W locus, XVII, Chapters 15, 17, 21, 29. Mutation at this locus is common. Homozygotes or compounds of the mutant alleles at this locus tend to develop ovarian tumors, a defect thought to be due to the absence of germ cells resulting in underproduction of sex hormone and overproduction of pituitary gonadotrophic hormone with excess stimulation of the gonad ( Russell and Fekete, 1958; Murphy and Russell, 1963). Alleles with published descriptions are:

See also MGI.

W, dominant spotting, semidominant. This is an old mutant of the mouse fancy. Heterozygotes have variable amounts of white spotting depending on the genetic background. Colored areas may be interspersed with white hairs to produce a roan type of pattern ( Dunn, 1937a). Heterozygotes have normal blood and are fully viable and fertile ( Grüneberg, 1942b). Homozygotes are white with black eyes in which the pigment is restricted to the retina. They have a severe macrocytic anemia and a severe shortage of primary germ cells ( Mintz and Russell, 1957). They die within the first week after birth. See also MGI.

W^a, Ames dominant spotting, semidominant. Found among offspring of an X-rayed male of the Z strain. Resembles W except that heterozygotes have a prominent blaze and more often have belly spotting. Homozygotes are anemic and die within a few days after birth ( Schaible, 1963c). See also MGI.

W^b, Ballantyne's spotting, semidominant. Arose in the C57/St strain. Heterozygotes are more extensively spotted than W^v/+ and the coat color is more diluted. Homozygotes may survive to maturity. They are anemic, black-eyed white, and sterile ( Ballantyne et al., 1961). See also MGI.

W^j, Jay's dominant spotting, semidominant. Arose spontaneously in the C3H strain. W^j resembles W in its effects in heterozygotes and homozygotes with the exception that it causes more white spotting in heterozygotes ( E.S. Russell et al., 1957). See also MGI.

W^v, viable dominant spotting, semidominant. Discovered by Little and Cloudman ( 1937) in the C57BL inbred strain. Heterozygotes have a variable amount of white spotting and also a slight dilution of the coat color. They have a slight macrocytic anemia ( E.S. Russell, 1949b) but are fully viable and fertile. Homozygotes resemble W/ W in color, anemia, and germ cells but many of them survive to maturity. W/W^v mice are also viable. W^v/W^v mice utilize the L form of several amino acids and excrete the D form, whereas normal mice utilize both the D and L forms. W^v/+ mice are intermediate in this respect ( Goodman, 1956; Chapter 19). See also MGI.

W^x, a mutant indistinguishable from W. It occurred in the C3H/HeJ strain in 1952 ( E.S. Russell et al., 1957; Murphy and Russell, 1963). See also MGI.

wa-1, waved-1, recessive, XI. Found in a mixed mouse colony ( Crew, 1933). Homozygotes are recognizable at 2 or 3 days of age by their curly whiskers. The first coat is strongly waved but the hair becomes straight in later coats. Most of the whiskers also become straight but the guard hairs are curved and shorter than normal. The hair follicles of the first coat are curved but the curvature disappears in later hair generations. The hairs are somewhat less keratinized than normal ( David, 1937). Bennett and Gresham ( 1956) found that many wa-1/wa-1 mice had eyelids open at birth and ascribed the condition to a closely linked gene, but the possibility that open eyelids is a pleiotropic effect of wa-1 was not excluded. See also MGI.

wa-2, waved-2, recessive, VII. Found in an "abnormal corpus callosum" stock ( Keeler, 1935). This mutant is very similar to wa-1. Homozygotes can be recognized at 2 to 3 days by their curly whiskers. The first coat is waved but later coats are not. The vibrissae usually remain curled and the guard hairs curved. Some homozygotes have eyelids open at birth ( Butler and Robertson, 1953; Green, unpublished). Butler and Robertson have ascribed the condition to an independent gene squint ( sq), but it was probably a pleiotropic effect of wa-2. See also MGI.

wd, waddler, recessive, VIII. Arose spontaneously in a stock carrying furless. Homozygotes can be identified at about 14 days of age. The hindquarters sway from side to side in a smooth arc and the mice often fall on their hips. No trembling or paralysis occurs. Homozygotes are smaller than their normal littermates from 3 weeks on, but viability is good and many waddlers are fertile. The abnormalities of behavior do not become more severe with age ( Yoon, 1959). Studies have been made of the serum proteins ( Yoon, 1961a), serum cholinesterase ( Yoon and Harris, 1962), and acid-soluble phosphorus ( Yoon and Denuccio, 1963) of the brain of wd/wd mice, but the results are not easily interpretable. See also MGI.

we, wellhaaring, recessive, V. Arose as a spontaneous mutation in the stocks of Agnes Bluhm. Homozygotes are fully fertile. They have curly whiskers at 2 or 3 days of age and a wavy first coat, most strongly evident between 10 and 21 days. In later coats the waviness is lost. The hairs have a lower average diameter than those of normal mice ( Hertwig, 1942). See also MGI.

wh, writher, recessive, linkage not known. This mutant is similar to dt, but has not been tested with it. Possibly radiation-induced. Affected mice die before weaning. They are unable to support themselves on their legs. Convulsions of the torso occur in later stages. The condition is first recognizable at 12 days ( Kelly, 1953). See also MGI.

wi, whirler, recessive, VIII. Arose as a spontaneous mutation in a multiple recessive stock. Viability may be slightly reduced. Both sexes are fertile but females do not always make good mothers. Homozygotes show the characteristic symptoms of the shaker syndrome, deafness, head-tossing, circling and hyperactivity ( Lane, 1963). They have defects of the membranous labyrinth similar to those of sh-2 (Deol, 1965, personal communication). Oxygen consumption and adrenal weight are greater than normal ( Sackler et al., 1964). See also MGI.

wl, wabbler-lethal, recessive, III. Arose in a stock carrying pirouette ( Dickie et al., 1952). Homozygotes are first recognizable at 12 days of age and usually die at about 4 weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. Difficulty in walking increases in severity until the animal dies. Histological examination shows myelin degeneration widely distributed throughout the central nervous system, particularly in the vesibulocerebellar and spinocerebellar systems ( Harman, 1954). The onset of demyelinization of individual tracts is in the same order as their myelinization. Axons are normal. The interfascicular glia show extensive atrophy in the tracts where abnormal myelin is present ( Anderson and Harman, 1961). Leukopenia is found from 2 weeks of age until death ( Mufson and Starr, 1958). See also MGI.

wr, wobbler, recessive, linkage not known. Arose in the C57BL/Fa strain. The main features are tremor and paralysis which affect the forelimbs more than the hind limbs. Penetrance appears to be complete, but both sexes are sterile and much reduced in viability ( Duchen et al., 1966). See also MGI.

Wt, waltzer-type, semidominant, linkage not known, Chapter 32. Arose spontaneously at the Oak Ridge National Laboratory. Heterozygotes may show nervous behavior varying from slight nervousness to rapid circling. They are not deaf. The posterior and lateral semicircular canals are abnormal, with defects ranging from slight shortening to complete absence distal to the ampulla. The rest of the labyrinth is normal. All Wt/+ mice appear to have morphological abnormalities of the labyrinth, but many of them do not show any behavioral abnormality. Circling behavior is associated with defective lateral rather than posterior canals. Both canals seem important for normal swimming, and a larger proportion of mice with defective canals can be detected on this basis. Wt/Wt mice die at about the 11th day of gestation ( Stein and Huber, 1960). See also MGI.

wv, weaver, recessive, linkage not known. Arose spontaneously in the C57BL/6J inbred strain. Homozygotes resemble staggerer and reeler mice but wv is not allelic with sg or rl. Affected mice do not live to maturity. Gross inspection of the brain shows that the cerebellum is defective ( Lane, 1964). See also MGI.

Xt, extra-toes, semidominant, XIV, Chapter 15. Probably X-ray-induced. Heterozygotes have extra toes on the preaxial side of the hind feet. Penetrance is nearly complete. On the front feet one or more preaxial digits may be lacking. Homozygotes die with cranioschisis and have many extra toes on all feet ( Lyon et al., 1964a). See also MGI.

Bacillus enteritidis resistance. It was shown by Webster ( 1937) that a single locus controls resistance to this bacterium. Alleles at this locus segregate independently of those at the locus controlling resistance to the Arbor B viruses. The allele for resistance is dominant to that for susceptibility. The BRVR strain is resistant and the BSVS strain is susceptible.

Arbor B virus resistance. A single locus with alleles controlling susceptibility and resistance to the Arbor B viruses has been demonstrated by Webster ( 1937) and Sabin ( 1952). Resistance seems to be a property of the macrophages, since macrophages from resistant mice do not support growth of the virus, whereas kidney and lung cultures from resistant mice, and macrophages from susceptible mice do ( Goodman and Koprowski, 1962). The allele for resistance is dominant to that for susceptibility. The PRI and BRVR strains are resistant and C3H/He is susceptible. This locus is probably independent of that controlling resistance to mouse hepatitis virus ( Kantoch et al., 1963).

Mouse hepatitis virus resistance. The C3H/An strain is resistant to mouse hepatitis virus and the PRI strain is susceptible. The difference is due to differences at one or possibly two loci with susceptibility dominant to resistance. Resistance or susceptibility is a property of the macrophages. Cultivation of resistant macrophages in a medium containing an extract of susceptible macrophages changes them to susceptible cells. Preliminary comparisons with Arbor B virus resistance based on tests of survivors of various backcrosses indicates that the two characters are independent ( Kantoch et al., 1963). See also MGI.

Leukencephalosis. A dystrophy of the white matter of the brain producing an ex vacuo hydrocephalus occurred in Hertwig's sy strain ( Fisher, 1959). It is recessive and appears to have full penetrance. The dystrophy begins in the occipital parts of the telencephalon and spreads nasad and laterad. Other parts of the brain are unaffected. This mutant is similar to cerebral degeneration ( cb) but has not been tested for allelism with it.

Neonatal jaundice. A recessive mutant causing jaundice in the newborn usually with death before 10 days has been described by Scheufler ( 1963). In the blood there are few normocytes, many polychromatic erythrocytes, sperocytes, poikilocytes, fragments, and a few erythroblasts. Hemoglobin is very deficient. One surviving homozygous female was fertile but no males were fertile. Not tested for allelism with ha, ja or sph.

Biosynthesis of corticosteroids. The in vitro synthesis of cortisol and corticosterone by the adrenal glands is about twice as high in strain A/Cam as in strain CBA/Fa. The difference appears to be controlled by a single locus with the allele in strain A dominant to that in strain CBA ( Badr and Spickett, 1965).

Linkage groups

The mouse has 20 pairs of chromosomes and should therefore have 20 linkage groups. Eighteen autosomal groups and a sex-linked group are known ( Figure 8-3 and Table 8-1). Linkage groups I, II, V, VII, VIII, IX, XI, XIII, XVII (formerly part of III, Lane, 1965), and XX have been shown by Slizynski ( 1954, 1957) to be on different chromosomes. VI, IX, XII, and XV are very short, and at least one end of X, XI, XVI, and perhaps some of the others has not been adequately tested against all other known linkage groups. It is therefore likely that some present assignments of loci will eventually be changed.

In Figure 8-3 the loci whose order is uncertain are shown in boldface. Brackets indicate that the order within the bracketed group has not been established. Where recombination differs in males and females, the unweighted average is given. The recombinations between adjacent loci have in many cases been determined directly, but in others the values were obtained by subtraction. The map is therefore not to be taken too literally.

Table 8-1 gives the recombination values between adjacent loci when these are known and some values between nonadjacent loci. Other recombination values that have been determined can be found in the references cited. Whenever recombination is different in the two sexes, the values for males and females are given separately. When there is no sex difference or when values were not determined for the sexes separately, only one value is given. In combining estimates from different experiments each estimate was weighted by the reciprocal of its variance.

Centromere position

The position of the centromere is not known with certainty for any mouse linkage groups. Most attempts to map the centromere make use of a phenomenon known as affinity.

Occasionally genes known to be located on different chromosomes behave in crosses as if they were loosely linked. Such a case was first noticed by Gates ( 1926) in a cross between Japanese waltzers and European laboratory mice. Michie and Wallace ( 1953) have reinvestigated the phenomenon. They have called it affinity and have offered the explanation that affinity is due to the presence in a cross of different states of homologous centromeres, such that nonhomologous chromosomes with centromeres of the same state tend to move to the same pole at meiosis rather than assort independently. Genes on nonhomologous chromosomes may thus appear to be linked. Wallace has made crosses which demonstrate association between markers in linkage groups V and III and has used the results to map the position of the centromere in linkage group V (Wallace, 1957a, 1958b, 1959, 1961). She concluded that it lies between fi and Sd. Parsons ( 1959) has found a possible case of affinity between linkage groups V and XIII and has suggested that the evidence favors the conclusion that the centromere in XIII is near Dh and ln. Michie, in his reanalysis of Gates's results ( Michie, 1955b) concluded that the centromere in linkage group II is near d.

These positions are all median or subterminal with respect to known markers in the three linkage groups. On cytological examination, however, the mitotic chromosomes of the mouse appear to have terminal centromeres ( Chapter 7, Levan et al., 1962), an observation in conflict with the results of affinity studies. It is possible that the centromeres are actually subterminal with a very short arm not easily seen with the light microscope. If a chiasma occurred with high frequency in the short arm, the genetic map of the arm would appear to be quite long. However, the observations of Ford and Evans ( 1964) on the position of chiasmata in ring bivalents at meiosis argue against the probability that chiasmata occur in the short arm with appreciable frequency. It seems safest, therefore, not to regard the position of the centromeres in linkage groups II, V, and XIII as established from affinity studies, but to reserve judgment until there is confirmation by other methods.

Evidence on the position of the centromere in linkage group IX is discussed in Chapter 24.

Since most named mutant genes have consistent and easily recognized effects not obscured by the normal range of variation in environment or genetic background, most of them can be maintained without attention to systematic breeding schemes. Many systematic schemes which are useful for various purposes have been devised, however. Consult Lyon ( 1963b) for a more comprehensive discussion of methods of maintaining mutants.

Inbred stocks

Methods for keeping a mutant and its normal allele segregating on an otherwise homozygous background, either by crossing to a standard inbred strain or by inbreeding with forced heterozygosis, are described in Chapter 2. They will not be further discussed here.

Balanced stocks

Inviable or infertile recessive mutants must be bred from heterozygous carriers. Since the heterozygous offspring of such matings are not distinguishable from homozygous normal mice except by breeding tests, maintenance of such mutants is difficult. If closely linked mutants are known, they can be used to help distinguish carriers of the mutant in question in so-called balanced stocks.

If r is an inviable recessive mutant with wild-type allele +, and a a closely linked recessive with wild-type allele +, matings of the type r +/+ a x r +/+ a will produce the nonrecombinant offspring r +/r + (homozygotes for r), + a/+ a (homozygotes for a), and r +/+ a (wild type carrying both r and a). In the absence of recombination, wild-type offspring mated together will again produce the same three types in the next generation. Recombination will cause some wild-type offspring to be r +/+ + or + +/+ a, but the closer the linkage the rarer will be such progeny. The stock can be propagated by mating wild-type animals together. If such matings produce both r +/r + and + a/+ a offspring, they are then proved to be of the expected type and their wild-type offspring can in turn be used to produce the next generation. Figure 8-4 shows the expected proportion of such matings which will be of the proper type for various degrees of linkage between r and a. It was noted in Chapter 2 that in propagating a recessive mutant by intercrosses, the probability that matings between the sibs of homozygous mutants will in fact be matings between heterozygotes is 2/3 x 2/3 or 4/9 (44 per cent). From Figure 8-4 it can be seen that use of a linked recessive marker will increase this probability only if it is closer than 17 map units to the mutant in question. A linked semidominant marker is somewhat more efficient. This is because the heterozygotes for the semidominant can be positively identified, thus eliminating half of the uncertainty in the selection of animals for mating.

D.S. Falconer (1965, personal communication) has pointed out that if small numbers of offspring are raised, the probability that a suitable mating will be recognized as such is somewhat lower for a balanced stock with a linked recessive marker than for a stock with a linked dominant or with no linked marker. This is because both mutants must be recovered in the stock with a linked recessive to prove that a mating is suitable, but only one must be recovered in stocks with a linked dominant or no linked marker. If as many as 12 offspring are obtained, however, the probability that a suitable mating will be discovered is 94 per cent in a stock with a linked recessive and 97 per cent in the other two cases. The dashed lines in Figure 8-4 show the proportion of matings that will be discovered to be suitable with 12 offspring for the three cases. I am indebted to Dr. Falconer for the method used in calculating these proportions. In practice it is usually easier to raise a second litter if the first one fails to prove a mating than to discard the mating and make up another one. The linked marker should be close enough and enough offspring should be produced to raise the proportion of suitable matings discovered to about 65 to 70 per cent to result in much saving of space.

An example of the use of a linked recessive marker is the case of wabbler lethal ( wl) balanced against hairless ( hr). Recombination between the two loci is about 4 per cent. Figure 8-4 shows that about 80 per cent of the matings will produce both wl/ wl and hr/ hr among 12 offspring and will therefore be suitable for propagating the stock. For practical purposes, considering that extra matings must be maintained to insure against sterility, this is very nearly as good as 100 per cent, and a great increase in efficiency over the 43 per cent of suitable matings obtained in maintaining wl by itself.

Another example is the use of the semidominant luxate ( lx) balanced against reeler ( rl). The recombination is about 16 per cent. About 65 per cent of matings between heterozygous luxate mice will therefore produce rl/ rl and be suitable for propagating the stock.

Balanced stocks are also useful for determining the effect of a mutant in both single and double dose. For a recessive mutant (r) this means that comparisons be made between +/+, +/r, and r/r. A closely linked marker (a) can be useful in distinguishing +/+ for, +/r. Among offspring of matings of r +/+ a x r +/+ a, those +/+ at the r locus will be + a/+ a, and recognizable as homozygotes for a, whereas those heterozygous at the r locus will be r +/+ a and recognizable as wild type for both r and a.

An example is the use of short ear ( se) in studies of the effect of dilute lethal ( d^l) on phenylalanine metabolism. Matings of d^l +/+ se x d^l +/+ se produce + se/+ se (short-eared, homozygous wild type for d^l), d^l +/+ se (wild type, heterozygous for d^l) and d^l +/ d^l +(homozygous for d^l). This linkage is very tight (recombination = 0.15 per cent) and identification is therefore virtually without error. Looser linkages may be useful if the effect under investigation is large enough. The linked marker must, of course, be known not to influence the effect in question.

Linked markers for early identification of a mutant

In studying the mode of action of a mutant gene during development it is often useful to know whether a mouse is the mutant type before any known effect of the gene is detectable. If the mutant is viable and fertile when homozygous, this can be achieved by mating homozygotes together. But for mutants which must be bred from heterozygotes and which therefore have non-mutant littermates, some means of identifying the mutants early may be very useful. Even in the case of fertile mutants it is often desirable to have nonmutant littermates as controls. If there exists a closely linked recessive or semidominant marker which is recognizable earlier in development than the mutant of interest, the phenotype of the marker can be used to identify the mutant individuals in offspring of appropriate matings. Table 8-2 shows some of the kinds of matings that can be used for various kinds of mutants, where r is a recessive mutant of interest, D is a dominant or semidominant mutant of interest, a is a linked recessive, and A is a linked semidominant.

This method has not been widely used in the mouse, in part because suitable markers have only rarely been available. E.S. Russell et al. ( 1956) were able to use the semidominant luxate ( lx) in coupling with W^v to identify W^v/ W^v and W^v/+ embryos at 12 days of gestation. Even a fairly loosely linked marker may be useful provided enough offspring can be examined to establish a correlation between the presence of the marker and the effect being examined. It may, of course, be necessary to establish by means of appropriate controls that the effect is not due to the marker itself. It should also be pointed out that it is not easy to put two closely linked recessives together in the same chromosome, particularly if one is lethal or sterile.

Linked dominant marker for crossing a recessive to an inbred strain

Transferring a recessive mutant to an inbred background requires a two-generation cross-intercross cycle, or, if the mutant is infertile, continued backcrossing with test crossing of the prospective parents in each generation ( Chapter 2). If a closely linked dominant marker is available, the intercross generation can be omitted and continued backcrossing used with a high probability that the animals backcrossed will be carrying the mutant of interest. Using the conventions of the previous section, matings of the type D r/+ + x + +/+ + produce D r/+ + and + +/+ +. The D r/+ + offspring are chosen and backcrossed again to the inbred strain.

This plan has been used to transfer the very deleterious mutant, anemia ( an), to the C57BL/6J background using the dominant marker, light ( B^lt). Recombination between the two loci is about 8 per cent, so that 92 per cent of the light offspring from matings of B^lt an/+ + x C57BL/6J will be carrying an ( B^lt an/+ +). It is wise to maintain several lines and to intercross light offspring in every generation or every other generation to make sure that the recessive has not been lost by recombination.

Multiple mutant stocks for linkage testing

Multiple linkage group stocks. For efficient testing of a new mutant to locate it on the linkage map it is desirable to have linkage testing stocks so designed that linkage with a maximum length of the known map can be tested with a minimum number of crosses. The first such stocks in the mouse were designed and produced by Snell ( Cooper, 1939). With many new mutants available, Carter and Falconer ( 1951) devised a new set of stocks and described the theory of their design. The theory allows the calculation of the length of linkage map tested and so makes possible comparison of the relative efficiency of different sets of stocks. Since 1951, new mutants and an extended linkage map have made various modifications of these stocks possible. Similar though not identical sets of stocks are now maintained in several laboratories. Lists of such stocks and the laboratories which maintain them are carried periodically in Mouse News Letter, a mimeographed bulletin produced and distributed by the International Committee on Laboratory Animals and the Laboratory Animals Centre, MRC Laboratories, Woodmansterne Road, Carshalton, Surrey, England.

The linkage testing stocks maintained at The Jackson Laboratory in 1965 are listed in Table 8-3. These stocks leave some large regions untested including the wa-2 end of VII and the bg end of XIV. Markers covering these regions are available in other stocks.

Instructions for the use of such stocks and for the statistical treatment of the results can be found in Carter and Falconer ( 1951). More extensive and general discussions of linkage methods may be found in Mather ( 1951) and Green ( 1963).

Single linkage group stocks.

Once a linkage has been detected for a new mutant, it is desirable to determine the linear order of the mutant with respect to other loci in the linkage group. If the loci are close together three-point backcrosses are usually necessary. If the loci are marked by recessive mutants, the mutants must be in coupling, i.e., on the same chromosome, to make backcrosses possible. Combining closely linked recessive mutants is a tedious process, and it is therefore useful to maintain whatever such combinations have been produced, to have them available for future use. Numerous such stocks are now in existence in various laboratories and can be found listed in Mouse News Letter. At The Jackson Laboratory stocks carrying at least two linked recessives in coupling are available for linkage groups I, II, III, IV, V, VII, VIII, XIII, XIV, and XVII.

The over 300 named mutant genes of the mouse, as well as a few conditions which have been shown to be due to mutants at as yet unnamed loci, are listed and briefly described. The known linkage groups are shown in a table with the pertinent recombination values. Efforts to map the positions of the centromeres by use of affinity are discussed.

Several kinds of stocks for maintaining mutants have been developed. Linked markers may be used to aid in the identification of carriers of recessive inviable or infertile mutants and to aid in the identification of a mutant early in development before any known effect of the mutant is detectable.

Multiple mutant stocks have been constructed for use in testing for linkage.

Allen, S.L. 1955. Linkage relations of the genes histocompatibility-2 and fused tail, brachyury and kinky tail in the mouse, as determined by tumor transplantation. Genetics 40: 627-650.
See also MGI.

Anderson, F.D., and P.J. Harman. 1961. Neurohistology of two mammalian mutations. Neurology 11: 676-680.
See also PubMed.

Arnesen, K. 1955. Constitutional difference in lipid content of adrenals in two strains of mice and their hybrids. Acta Endocrinol. 18: 396-401.
See also PubMed.

Arnesen, K. 1956. The Adrenothymic Constitution and Susceptibility to Leukemia in Mice; a Study of the AKR/O and WLO Strains and their Hybrids. Acta Pathol. Microbiol. Scand. Suppl. 109. 95 p.
See also PubMed.

Arnesen, K. 1963. The cytology of the adrenal cortex in mice with spontaneous adrenocortical lipid depletion. Acta Pathol. Microbiol. Scand. 58: 212-218.
See also MGI.

Ashton, G.C., and A.W.H. Braden. 1961. Serum β-globulin polymorphism in mice. Austral. J. Biol. Sci. 14: 248-253.
See also MGI.

Auerbach, C., D.S. Falconer, and J.H. Isaacson. 1962. Test for sex-linked lethals in irradiated mice. Genet. Res. 3: 444-447.
See also MGI.

Auerbach, R. 1954. Analysis of the developmental effects of a lethal mutation in the house mouse. J. Exp. Zool. 127: 305-329.
See also MGI.

Badr, F.M., and S.G. Spickett. 1965. Genetic variation in the biosynthesis of corticosteroids in Mus musculus. Nature 205: 1088-1090.
See also PubMed.

Ballantyne, J., F.G. Bock, L.C. Strong, and W.C. Quevedo, Jr. 1961. Another allele at the W locus of the mouse. J. Hered. 52: 200-202.
See also MGI.

Barber, A.N. 1957. The effects of maternal hypoxia on inheritance of recessive blindness in mice. Amer. J. Ophthalmol. 44: 94-101.
See also MGI.

Barnicot, N.A. 1945. Some data on the effect of parathormone on the grey-lethal mouse. J. Anat. 79: 83-91.
See also PubMed.

Barnicot, N.A. 1948. The local action of the parathyroid and other tissues on bone in inracerebral grafts. J. Anat. 82: 233-248.
See also PubMed.

Bartke, A. 1964. Histology of the anterioir hypophysis, thyroid and gonads of two types of dwarf mice. Anat. Rec. 149: 225-235.
See also MGI.

Bartke, A. 1965. Mouse News Letter 32: 52-53.
See also MGI.

Bateman, N. 1954. Bone growth: a study of the grey-lethal and microphthalmic mutants of the mouse. J. Anat. 88: 212-262.
See also MGI.

Bateman, N. 1957. Mouse News Letter 16: 7.
See also MGI.

Bateman, N. 1960. High frequency of a lethal gene (t^e) in a laboratory stock of mice. Genet. Res. 1: 214-225.

Bateman, N. 1961. Sombre, a viable dominant mutant in the house mouse. J. Hered. 52: 186-190.
See also MGI.

Batt, R.A.L., and G.A. Harrison. 1963. The reproductive system of the adipose mouse. J. Hered. 54: 135-138.
See also PubMed.

Beasley, A.B. 1963. Inheritance and development of a lens abnormality in the mouse. J. Morphol. 112: 1-11.
See also MGI.

Beck, S.L. 1963a. The anophthalmic mutant of the mouse. I. Genetic contribution to the anophthalmic phenotype. J. Hered. 54: 39-44.
See also MGI.

Beck, S.L. 1963b. The anophthalmic mutant of the mouse. II. An association of anophthalmia and polydactyly. J. Hered. 54: 79-83.
See also MGI.

Beck, S.L. 1963c. Frequencies of teratologies among homozygous normal mice compared with those heterozygous for anophthalmia. Nature 200: 810-811.
See also MGI.

Bennett, D. 1956. Developmental analysis of a mutation with pleiotropic effects in the mouse. J. Morphol. 98: 199-234.
See also MGI.

Bennett, D. 1958. In vitro study of cartilage induction in T/T mice. Nature 181: 1286.
See also MGI.

Bennett, D. 1959. Brain hernia, a new recessive mutation in the mouse. J. Hered. 50: 265-268.
See also MGI.

Bennett, D. 1961a. A chromatographic study of abnormal urinary amino acid excretion in mutant mice. Ann. Hum. Genet. 25: 1-6.
See also MGI.

Bennett, D. 1961b. Miniature, a new gene for small size in the mouse. J. Hered. 52: 95-98.
See also MGI.

Bennett, D., S. Badenhausen, and L.C. Dunn. 1959. The embryological effects of four late-lethal t-alleles in the mouse which affect the neural tube and skeleton. J. Morphol. 105: 105-143.
See also PubMed.

Bennett, J.H., and G.A. Gresham, 1956. A gene for eyelids open at birth in the house mouse. Nature 178: 272-273.
See also MGI.

Bernstein, S.E. 1960. Mouse News Letter 23: 33.
See also MGI.

Bernstein, S.E. 1963. Analysis of gene action and characterization of a new hematological abnormality, hemolytic anemia, p. 186. In S.J. Geerts [ed.] Proc. XI Int. Congr. Genet. Vol. 1. Pergamon Press, New York. (Abstr.)
See also MGI.

Berry, R.J. 1960. Genetical studies on the skeleton of the mouse. XXVI. Pintail. Genet. Res. 1: 439-451
See also MGI.

Berry, R.J. 1961a. The inheritance and pathogenesis of hydrocephalus-3 in the mouse. J. Pathol. Bacteriol. 81: 157-167.
See also MGI.

Berry, R.J. 1961b. Genetically controlled degeneration of the nucleus pulposus in the mouse. J. Bone Joint Surg. 43B: 387-393.
See also MGI.

Bhaskar, S.N., I. Schour, E.C. MacDowell, and J. P. Weinmann. 1951. The skull and dentition of screw tail mice. Anat. Rec. 110: 199-229.
See also MGI.

Bielschowsky, M., and G.C. Schofield. 1962. Studies on megacolon in piebald mice. Austral. J. Exp. Biol. Med. Sci. 40: 395-404.
See also MGI.

Bierwolf, D. 1956. Kleinhirnmissbildungen durch hereditaren Hydrocephalus bei der Hausmaus. Wiss. Z. Martin-Luther-Univ. 5: 1237-1282.

Bierwolf, D. 1958. Die Embryogenese des Hydrocephalus und der Kleinhirnmissbildungen beim Dreherstamm der Hausmaus. Morphol. Jahrb. 99: 542-612.
See also MGI.

Billingham, R.E., and W.K. Silvers. 1960. The melanocytes of mammals. Quart. Rev. Biol. 35: 1-40.
See also MGI.

Bloom, J.L. 1962. Mouse News Letter 27: 30.

Bloom, J.L., and D.S. Falconer. 1964. A gene with major effect on susceptibility to induced lung tumors in mice. J. Nat. Cancer Inst. 33: 607-618.
See also MGI.

Bodmer, W.F. 1961. Viability effects and recombination differences in a linkage test with pallid and fidget in the house mouse. Heredity 16: 485-495.
See also MGI.

Bonnevie, K. 1936. Abortive differentiation of the ear vesicles following a hereditary brain-anomaly in the "short-tailed waltzing mice." Genetica 18: 105-125.
See also MGI.

Bonnevie, K., and A. Brodal. 1946. Hereditary hydrocephalus in the house mouse. IV. The development of the cerebellar anomalies during foetal life with notes on the normal development of the mouse cerebellum. Skr. Norske Vidensk.-Akad. Oslo, I. Mat.-Nutur. Kl. 1946 (4). 60 p.
See also MGI.

Boyse, E.A., L.J. Old, and S. Luell. 1964. Genetic determination of the TL (thymus-leukaemia) antigen in the mouse. Nature 201: 779.
See also MGI.

Braden, A.W.H., and S. Gluecksohn-Waelsch, 1958. Further studies of the effect of the T locus in the house mouse on male fertility. J. Exp. Zool. 138: 431-452.
See also PubMed.

Braverman, I.M. 1953. Neurological actions caused by the mutant gene "trembler" in the house mouse (Mus musculus, L.): an investigation. J. Neuropathol. Exp. Neurol. 12: 64-72.
See also PubMed.

Brooke, H.C. 1926. Hairless mice. J. Hered 17: 173-174.
See also MGI.

Brückner, R. 1951. Spaltlampenmikroskopie and Ophthalmoskopie am Auge von Ratte und Maus. Doc. Ophthalmol. 5-6: 452-554.
See also MGI.

Bryson, V. 1945. Development of the sternum in screw tail mice. Anat. Rec. 91: 119-141.
See also MGI.

Bunker, H., and G.D. Snell. 1948. Linkage of white and waved-1. J. Hered. 39: 28.
See also MGI.

Bunker, L.E. 1959. Hepatic fusion, a new gene in linkage group I of the mouse. J. Hered. 44: 13-16.
See also MGI.

Butler, L. and D.A. Robertson. 1953. A new eye abnormality in the house mouse. J. Hered. 44: 13-16.
See also MGI.

Carter, T.C. 1947. A new linkage in the house mouse: undulated and agouti. Heredity 1: 367-372.
See also MGI.

Carter, T.C. 1948. A new strain of luxate mice. Heredity 2: 405-406. (Abstr.)

Carter, T.C. 1951a. The position of fidget in linkage group V of the house mouse. J. Genet. 50: 264-267.
See also MGI.

Carter, T.C. 1951b. Wavy-coated mice: phenotypic interactions and linkage tests between rex and (a) waved-1, (b) waved-2. J. Genet. 50: 268-276.
See also MGI.

Carter, T.C. 1951c. The genetics of luxate mice. I. Morphological abnormalities of heterozygotes and homozygotes. J. Genet. 50: 277-299.
See also MGI.

Carter, T.C. 1951d. The genetics of luxate mice. II. Linkage and independence. J. Genet. 50: 300-306.
See also MGI.

Carter, T.C. 1953. The genetics of luxate mice. III. Horsheshoe kidney, hydronephrosis and lumbar reduction. J. Genet. 51: 441-457.
See also MGI.

Carter, T.C. 1954. The genetics of luxate mice. IV. Embryology. J. Genet. 52: 1-35.
See also MGI.

Carter, T.C. 1956. Genetics of the Little and Bagg X-rayed mouse stock. J. Genet. 54: 311-326.
See also MGI.

Carter, T.C. 1959a. Mouse News Letter 21: 40.
See also MGI.

Carter, T.C. 1959b. Embryology of the Little and Bagg X-rayed mouse stock. J. Genet. 56: 401-435.
See also MGI.

Carter, T.C., and D.S. Falconer. 1951. Stocks for detecting linkage in the mouse, and the theory of their design. J. Genet. 50: 307-323.

Carter, T.C., M.F. Lyon, R.J. Phillips and B.M. Slizynski, 1954. Partial sex linkage in the mouse. Nature 174: 309-310.
See also PubMed.

Carter, T.C., and R.S. Phillips. 1950. Icthyosis, a new recessive mutant in the house mouse. J. Hered. 41: 297-300.
See also MGI.

Carter, T.C., and R.J.S. Phillips. 1953. The sex distribution of waved-2, shaker-2, and rex in the house mouse. Z. Indukt. Abstamm. Vererb. 85: 564-578.
See also MGI.

Carter, T.C., and R.J.S. Phillips. 1954. Ragged, a semidominant coat texture mutant in the house mouse. J. Hered. 45: 151-154.
See also MGI.

Caspari, E., and P.R. David. 1940. The inheritance of a tail abnormality in the house mouse. J. Hered. 31: 427-431.
See also MGI.

Chai, C.K. 1961. Hereditary spasticity in mice. J. Hered. 52: 241-243.
See also MGI.

Chai, C.K., E. Roberts, and R.L. Sidman. 1962. Influence of aminooxyacetic acid, a γ-aminobutyrate transaminase inhibitor, on hereditary spastic defect in the mouse. Proc. Soc. Exp. Biol. Med. 109: 491-495.
See also MGI.

Chase, H.B. 1942. Studies on an anophthalmic strain of mice. III. Results of crosses with other strains. Genetics 27: 3390348.
See also PubMed.

Chase, H.B. 1944. Studies on an anophthalmic strain of mice. IV. A second major gene for anophthalmia. Genetics 29: 264-269.
See also MGI.

Chesley, P. 1935. Development of the short-tailed mutant in the house mouse. J. Exp. Zool. 70: 429-459.
See also MGI.

Christophe, J. 1963. Biochemie des obésités expérimentales. Prob. Actuel. Endocrinol. Nutr. 7: 23-76.

Cinader, B., S. Dubiski, and A.C. Wardlaw. 1964. Distribution, inheritance, and properties of an antigen, MuB1, and its relation to hemolytic complement. J. Exp. Med. 120: 897-924.
See also MGI.

Clark, F.H. 1932. Hydrocephalus, a hereditary character in the house mouse. Proc. Nat. Acad. Sci. 18: 654-656.
See also MGI.

Clark, F.H. 1934. Anatomical basis of a hereditary hydrocephalus in the house mouse. Anat. Rec. 58: 225-233.
See also MGI.

Clark, F.H. 1935. Two hereditary types of hydrocephalus in the house mouse (Mus musculus). Proc. Nat. Acad. Sci. 21: 150-152.
See also MGI.

Cloudman, A.M., and L.E. Bunker. 1945. The varitint-waddler mouse. A dominant mutation in Mus musculus. J. Hered. 36: 258-263.
See also MGI.

Coggeshall, R.E., C.J. D'Amato, M.A. Brobine, and S.P. Hicks. 1961. Developmental neuropathology of genetic mutant mouse "paralytic." Fed. Proc. 20: 330. (Abstr.)

Cohen, B.L. 1960. Genetics of plasma transferrins in the mouse. Genet. Res. 1: 431-438.
See also MGI.

Cohen, B.L., and D.C. Shreffler. 1961. A revised nomenclature for the mouse transferrin locus. Genet. Res. 2: 306-308.
See also MGI.

Coleman, D.L. 1960. Phenylalanine hydroxylase activity in dilute and nondilute strains of mice. Arch. Biochem. Biophys. 91: 300-306.
See also PubMed.

Coleman, D.L. 1962. Effect of genic substitution on the incorporation of tyrosine into the melanin of mouse skin. Arch. Biochem. Biophys. 69: 562-568.
See also MGI.

Cooper, C.B. 1939. A linkage between naked and caracul in the house mouse. J. Hered. 30: 212.
See also MGI.

Crew, F.A.E. 1933. Waved: an autosomal recessive coat form character in the mouse. J. Genet. 27: 95-96.
See also MGI.

Crew, F.A.E., and C. Auerbach. 1939. Rex: a dominant autosomal monogenic coat texture character in the mouse. J. Genet. 38: 341-344.
See also MGI.

Crew, F.A.E., and L. Mirskaia. 1931. The character "hairless" in the mouse. J. Genet. 25: 17-24.
See also MGI.

Cupp, M.B. 1958. Mouse News Letter 19: 37.
See also MGI.

Cupp, M.B. 1960. Mouse News Letter 22: 50.
See also MGI.

Cupp, M.B. 1962. Mouse News Letter 26: 51.
See also MGI.

Curry, G.A. 1959. Genetical and developmental studies of droopy-eared mice. J. Embryol. Exp. Morphol. 7: 39-65.
See also MGI.

Dagg, C.P., D.L. Coleman, and G.M. Fraser. 1964. A gene affecting the rate of pyrimidine degradation in mice. Genetics 49: 979-989.
See also MGI.

Danforth, C.H. 1958. The occurrence and genetic behavior of duplicate lower incisors in the mouse. Genetics 43: 139-148.
See also MGI.

David, L.T. 1932. The external expression and comparative dermal histology of hereditary hairlessness in mammals. Z. Zellforsch. 14: 616-719.
See also MGI.

David, L.T. 1937. Die gegenseitige Beeinflussung der Erbfaktoren für Haarlosigkeit und Welligkeit bei der Hausmaus (Mus musculus). Rev. Suisse Zool. 44: 397-400.

Deol, M.S. 1954. The anomalies of the labyrinth of the mutants varitint-waddler, shaker-2, and jerker in the mouse. J. Genet. 52: 562-588.
See also MGI.

Deol, M.S. 1956a. A gene for uncomplicated deafness in the mouse. J. Embryol. Exp. Morphol. 4: 190-195.
See also MGI.

Deol, M.S. 1956b. The anatomy and development of the mutants pirouette, shaker-1, and waltzer in the mouse. Proc. Roy. Soc. B 145: 206-213.
See also MGI.

Deol, M.S. 1961. Genetical studies on the skeleton of the mouse. XXVIII. Tail-short. Proc. Roy. Soc. B 155: 78-95.
See also MGI.

Deol, M.S. 1963. The development of the inner ear in mice homozygous for shaker-with-syndactylism. J. Embryol. Exp. Morphol. 11: 493-512.
See also MGI.

Deol, M.S. 1964a. The abnormalities of the inner ear in kreisler mice. J. Embryol. Exp. Morphol. 12: 475-490.
See also MGI.

Deol, M.S. 1964b. The origin of the abnormalities of the inner ear in dreher mice. J. Embryol. Exp. Morphol. 12: 727-733.
See also MGI.

Deol, M.S., and W. Kocher. 1958. A new gene for deafness in the mouse. Heredity 12: 463-466.
See also MGI.

Deol, M.S., and M.W. Robins. 1962. The spinner mouse. J. Hered. 53: 133-136.
See also MGI.

Deol, M.S., and G.M. Truslove. 1963. A new gene causing cerebral degeneration in the mouse, p. 183-184. In S.J. Geerts [ed.] Proc. XI Int. Congr. Genet. Vol. 1. Pergamon Press, New York. (Abstr.)
See also MGI.

DeOme, K.B. 1945. A new recessive lethal mutation in mice. Univ. Calif. Pub. Zool. 53: 41-66.
See also MGI.

Detlefsen, J.A. 1921. A new mutation in the house mouse. Amer. Natur. 55: 469-473.
See also MGI.

Detlefsen, J.A. 1925. The linkage of dark-eye and color in mice. Genetics 10: 17-32.
See also MGI.

Detlefsen, J.A., and L.S. Clemente. 1924. Linkage of a dilute color factor and dark eye in mice. Genetics 9: 247-260.
See also MGI.

Dickie, M.M. 1954. The tortoise shell house mouse. J. Hered. 45: 158-190.
See also MGI.

Dickie, M.M. 1955. Alopecia, a dominant mutation in the house mouse. J. Hered. 46: 31-34.
See also MGI.

Dickie, M.M. 1961. Mouse News Letter 25: 36.
See also MGI.

Dickie, M.M. 1962a. A new viable yellow mutation in the house mouse. J. Hered. 53: 84-86.
See also MGI.

Dickie, M.M. 1962b. Mouse News Letter 27: 37.
See also MGI.

Dickie, M.M. 1963. Mouse News Letter 29: 39.
See also MGI.

Dickie, M.M. 1964a. New splotch alleles in the mouse. J. Hered. 55: 97-101.
See also MGI.

Dickie, M.M. 1964b. Mouse News Letter 30: 30.
See also MGI.

Dickie, M.M. 1965. Mouse News Letter 32: 43-46.
See also MGI.

Dickie, M.M., J. Schneider, and P.J. Harman. 1952. A juvenile wabbler-lethal in the house mouse. J. Hered. 43: 283-286.
See also MGI.

Dickie, M.M., and G.W. Woolley. 1946. Linkage studies with the pirouette gene in the mouse. J. Hered. 37: 335-337.
See also MGI.

Dickie, M.M., and G.W. Woolley. 1950. Fuzzy mice. J. Hered. 41: 193-196.
See also MGI.

Dobrovolskaïa-Zavadskaïa, N. 1927. Sur la mortification spontanée de la queue chez la souris nouveau-née et sur l'existence d'une caracter hereditaire "non-viable." Compt. Rend. Soc. Biol. 97: 114-116.

Dobrovolskaïa-Zavadskaïa, N. 1928. L'irradiation des testicules et l'hérédite chez la souris. Arch Biol. 38: 457-501.

Dray, S., R. Lieberman, and H. A. Hoffman. 1963. Two murine γ-globulin allotypic specificities identified by ascitic fluid isoprecipitins and determined by allelic genes. Proc. Soc. Exp. Biol. Med. 113: 509-513.

Dubiski, S. and B. Cinader. 1963. A new allotype specificity in the mouse (MuA2). Nature 197: 705.
See also PubMed.

Duchen, L.W., D.S. Falconer, and S.J. Strich. 1966. Hereditary progressive neurogenic muscular atrophy in the mouse. J. Physiol. In press.

Duchen, L.W., S.J. Strich, and D.S. Falconer. 1964. Clinical and pathological studies of an hereditary neuropathy in mice (dystonia musculorum). Brain 87: 367-378.
See also MGI.

Dunn, L.C. 1928. A fifth allelomorph in the agouti series of the house mouse. Proc. Nat. Acad. Sci. 14: 816-819.
See also MGI.

Dunn, L.C. 1934. A new gene affecting behavior and skeleton in the house mouse. Proc. Nat. Acad. Sci. 20: 230-232.
See also MGI.

Dunn, L.C. 1937a. Studies on spotting patterns. II. Genetic analysis of variegated spotting in the house mouse. Genetics 22: 43-64.
See also MGI.

Dunn, L.C. 1937b. Caracul, a dominant mutation. J. Hered. 28: 334.
See also MGI.

Dunn, L.C. 1945. A new eye color mutant in the mouse with asymmetrical expression. Proc. Nat. Acad. Sci. 31: 343-346.
See also MGI.

Dunn, L.C., A.B. Beasley, H. Tinker. 1960. Polymorphisms in populations of wild house mice. J. Mammal. 41: 220-229.
See also MGI.

Dunn, L.C., D. Bennett, and A.B. Beasley. 1962. Mutation and recombination in the vicinity of a complex gene. Genetics 47: 285-303.
See also MGI.

Dunn, L.C., and E. Caspari. 1945. A case of neighboring loci with similar effects. Genetics 30: 543-568.
See also MGI.

Dunn, L.C., and D.R. Charles. 1937. Studies on spotting patterns. I. Analysis of quantitative variations in the pied spotting of the house mouse. Genetics 22: 14-42.
See also MGI.

Dunn, L.C., and S. Gluecksohn-Schoenheimer. 1942. Stub, a new mutation in the mouse. J. Hered. 33: 235-239.
See also MGI.

Dunn, L.C., and S. Gluecksohn-Schoenheimer. 1947. A new complex of hereditary abnormalities in the house mouse. J. Exp. Zool. 104: 25-51.
See also MGI.

Dunn, L.C., S. Gluecksohn-Schoenheimer, and V. Bryson. 1940. A new mutation in the mouse affecting spinal column and urogenital system. J. Hered. 31: 343-348.
See also MGI.

Dunn, L.C., and S. Gluecksohn-Waelsch. 1954. A genetical study of the mutation "fused" in the house mouse with evidence concerning its allelism with a similar mutation "kink." J. Genet. 52: 383-391.
See also MGI.

Dunn, L.C., and J. Mohr. 1952. An association of hereditary eye defects with white spotting. Proc. Natl. Acad. Sci. 38: 872-875.
See also MGI.

Dunn, L.C., and L.W. Thigpen. 1930. The silver mouse, a recessive color variation. J. Hered. 21: 495-498.
See also MGI.

Eaton, G.J., and M.M. Green. 1963. Giant cell differentiation and lethality of homozygous yellow mouse embryos. Genetica 34: 155-161.
See also MGI.

Elftman, H., and O. Wegelius. 1959. Anterior pituitary cytology of the dwarf mouse. Anat. Rec. 135: 43-49.
See also MGI.

Fahey, J.L., J. Wunderlich, and R. Mishell. 1964. The immunoglobulins of mice. II. Two subclasses of mouse 7S_γ2-globulins: _γ2a- and _γ2b-globulins. J. Exp. Med. 120: 243-251.
See also PubMed.

Falconer, D.S. 1947. Linkage of rex with shaker-2 in the house mouse. Heredity 1: 133-135.
See also MGI.

Falconer, D.S. 1950. Mouse News Letter 2: 3.
See also MGI.

Falconer, D.S. 1951. Two new mutants "trembler" and "reeler," with neurological actions in the house mouse. J. Genet. 50: 192-201.
See also MGI.

Falconer, D.S. 1952. Location of "reeler" in linkage group III in the mouse. Heredity 6: 255-257.
See also MGI.

Falconer, D.S. 1953. Total sex-linkage in the house mouse. Z. Indukt. Abstamm. Vereb. 85: 210-219.
See also MGI.

Falconer, D.S. 1954. Linkage in the mouse: the sex-linked genes and "rough." Z. Indukt. Abstamm. Vererb. 86: 263-268.
See also MGI.

Falconer, D.S. 1956. Mouse News Letter 15: 23.
See also MGI.

Falconer, D.S. 1957. Mouse News Letter 17: 40.
See also MGI.

Falconer, D.S. 1961. Mouse News Letter 25: 30.
See also MGI.

Falconer, D.S., and S.P. Flanagan. 1963. Mouse News Letter 29: 30.

Falconer, D.S., A.S. Fraser, and J.W.B. King. 1951. The genetics and development of "crinkled," a new mutant in the house mouse. J. Genet. 50: 324-344.
See also MGI.

Falconer, D.S., and J.H. Isaacson. 1959. Adipose, a new inherited obesity of the mouse. J. Hered. 50: 290-292.
See also MGI.

Falconer, D.S., and J.H. Isaacson. 1962a. The genetics of sex-linked anaemia in the mouse. Genet. Res. 3: 248-250.
See also MGI.

Falconer, D.S., and J.H. Isaacson. 1962b. Mouse News Letter 27: 30.
See also MGI.

Falconer, D.S., and J.H. Isaacson. 1965. Mouse News Letter 32: 30-31.
See also MGI.

Falconer, D.S., M. Latyszewski, and J.H. Isaacson. 1964. Diabetes insipidus associated with oligosyndactyly in the mouse. Genet. Res. 5: 473-488.
See also MGI.

Falconer, D.S., and U. Sierts-Roth. 1951. Dreher, ein neus Gen der Tangmausgruppe bei der Hausmaus. Z. Induct Abstamm. Vereb. 84: 71-73.
See also MGI.

Falconer, D.S., and G.D. Snell. 1952. Two new hair mutants, rough and frizzy, in the house mouse. J. Hered. 43: 53-57.
See also MGI.

Falconer, D.S., and W.R. Sobey. 1953. The location of "trembler" in linkage group VII. J. Hered. 49: 159-160.
See also MGI.

Feldman, H.W. 1922. A fourth allelomorph in the albino series in mice. Amer. Natur. 56: 573-574.
See also MGI.

Fielder, J.H. 1952. The taupe mouse. A new coat color mutation. J. Hered. 43: 75-76.
See also MGI.

Finlayson, J.S., M. Potter, and C.C. Runner. 1963. Electrophoretic variation and sex dimorphism of the major urinary protein complex in inbred mice: a new genetic marker. J. Nat. Cancer Inst. 31: 91-107.
See also MGI.

Fisher, H. 1956. Morphologishe und mikroshopisch-anatomische Untersuchen am Innenohr eines Stammes Spontanmutierter Häusmause (dreher). Z. Mikroskop.-Anat. Forsch. 62: 348-406.

Fisher, H. 1958. Die Embryogenese der Innenohrmissbildungen bei dem spontanmutierten Dreherstamm der Hausmaus. Z. Mikroscop.-Anat. Forsch. 64: 476-497.

Fisher, H. 1959. Mikroscopische Untersuchungen am Gehirn einer neuen Hausmausmutante mit Leukpdystrophie. Verhandl. Deut. Zool. Ges. Münster/Westf. 1959: 519-524.

Fisher, R.A. 1953. The linkage of polydactyly with leaden in the house mouse. Heredity 7: 91-95.
See also MGI.

Fisher, R.A., and W. Landauer, 1953. Sex differences of crossing over in close linkage. Amer. Natur. 87: 116.
See also MGI.

Fisher, R.A., M. F. Lyon, and A.R.G. Owen. 1947. The sex chromosome in the house mouse. Heredity 1: 355-366.
See also MGI.

Fitch, N. 1957. An embryological analysis of two mutants in the house mouse, both producing cleft palate. J. Exp. Zool. 136: 329-357.
See also MGI.

Fitch, N. 1961a. A mutation in mice producing dwarfism, brachycephaly, cleft palate and micromelia. J. Morphol. 109: 141-149.
See also MGI.

Fitch, N. 1961b. Development of cleft palate in mice homozygous for the shorthead mutation. J. Morphol. 109: 151-157.
See also MGI.

Flanagan, S.P. 1964. Mouse News Letter 31: 21.

Foerster, E. 1956. Mouse News Letter 14: 23.
See also MGI.

Ford, C.E., and E.P. Evans. 1964. A reciprocal translocation in the mouse between the X chromosome and a short autosome. Cytogenetics 3: 295-305.
See also PubMed.

Forsthoefel, P.F. 1958. The skeletal effects of the luxoid gene in the mouse, including its interactions with the luxate gene. J. Morphol. 102: 247-287.
See also MGI.

Forsthoefel, P.F. 1959. The embryological development of the skeletal effects of the luxoid gene in the mouse, including its interactions with the luxate gene. J. Morphol. 104: 89-141.
See also MGI.

Forsthoefel, P.F. 1962. Genetics and manifold effects of Strong's luxoid gene in the mouse, including its interactions with Green's luxoid and Carter's Luxate genes. J. Morphol. 110: 391-420.
See also MGI.

Forsthoefel, P.F. 1963. The embryological development of the effects of Strong's luxoid gene in the mouse. J. Morphol. 113: 427-451.
See also MGI.

Fraser, A.S., S. Sobey, and C.C. Spicer. 1953. Mottled, a sex-modified lethal in the house mouse. J. Genet. 51: 217-221.

Fraser, F.C. 1946. The expression and interaction of hereditary factors producing hypotrichosis in the mouse: histology and experimental results. Can. J. Res. D. 24: 10-25.
See also MGI.

Fraser, F.C., and M.L. Herer. 1948. Lens rupture, a new recessive gene in the house mouse. J. Hered. 39: 149.

Fraser, F.C., and M.L. Herer. 1950. The inheritance and expression of the "lens rupture" gene in the house mouse. J. Hered. 39: 149.
See also MGI.

Fraser, F.C., and G. Schabtach. 1962. "Shrivelled," a hereditary degeneration of the Lens in the house mouse. Genet. Res. 3: 383-387.

Freye, H. 1954. Anatomische und entwicklungsgeschlichtliche Untersuchungen am Skelett normaler und oligodactyler Maüse. Wiss. Z. Martin-Luther-Univ. 3: 801-824.
See also MGI.

Freye, H. 1956. Untersuchen über die Zahnanomalie des Mikrophthalmus-syndrome der Hausmaus. Z. Mensch. Vereb. Konst. 33: 492-504.
See also PubMed.

Garber, E.D. 1952a. Bald, a second allele of hairless in the house mouse. J. Hered. 43: 45-46.
See also MGI.

Garber, E.D. 1952b. "Bent tail," a dominant, sex-linked mutation in the mouse. Proc. Natl. Acad. Sci. 38: 876-879.
See also MGI.

Gates, A.H., and M. Karasek. 1965. Hereditary absence of sebaceous glands in the mouse. Science 148: 1471-1473.
See also MGI.

Gates, W.H. 1926. The Japanese waltzing mouse; its origin, heredity, and relation to the genetic characters of other varieties of mice. Pub. Carnegie Inst. Wash. No. 337: 83-138.

Gates, W.H. 1928. Linkage of the factors for short-ear and density in the house mouse. Genetics 13: 170-179.
See also MGI.

Gates, W.H. 1931. Linkage of the factor shaker with albinism and pink-eye in the house mouse. Z. Indukt. Abstamm. Vererb. 59: 220-226.
See also MGI.

Gluecksohn-Schoenheimer, S. 1943. The morphological manifestations of a dominant mutation in mice affecting tail and urogenital system. Genetics 28: 341-348.

Gluecksohn-Schoenheimer, S. 1949. The effects of a lethal mutation responsible for duplications and twinning in mouse embryos. J. Exp. Zool. 110: 47-76.
See also MGI.

Gluecksohn-Waelsch, S. 1961. Mouse News Letter 25: 12.
See also MGI.

Gluecksohn-Waelsch, S. 1963. Lethal genes and analysis of differentiation. Science 142: 1269-1276.

Gluecksohn-Waelsch, S., D. Hagedorn, and B.F. Sisken. 1956. Genetics and morphology of a recessive mutation in the house mouse affecting head an limb skeleton. J. Morphol. 99: 465-479.
See also MGI.

Gluecksohn-Waelsch, S., and S.A. Kamell. 1955. Physiological investigations of a mutation in mice with pleiotropic effects. Physiol. Zool. 28: 68-73.
See also MGI.

Gluecksohn-Waelsch, S., H.M. Ranney, and B.F. Siskin. 1957. The hereditary transmission of hemoglobin differences in mice. J. Clin. Invest. 36: 753-756.

Gluecksohn-Waelsch, S., and T.R. Rota. 1963. Development in organ tissue culture of kidney rudiments from mutant mouse embryos. Develop. Biol. 7: 432-444.
See also MGI.

Goodman, G., and H. Koprowski. 1962. Macrophages as a cellular expression of inherited natural resistance. Proc. Nat. Acad. Sci. 48: 160-165.
See also PubMed.

Goodman, R.M., 1956. The effect of the W^v allele in the mouse on the differential excretion of the optical isomers of several amino acids. J. Exp. Zool. 132: 189-217.
See also PubMed.

Goodwins, I.R., and M.A.C. Vincent. 1955. Further data on linkage between short-ear and Maltese dilution in the house mouse. Heredity 9: 413-414.
See also MGI.

Gower, J.S. 1953. Mouse News Letter 8, Suppl. 14.
See also MGI.

Gower, J.S. 1957. Mouse News Letter 16: 37.
See also MGI.

Gower, J.S., and M.B. Cupp. 1958. Mouse News Letter 19: 37.
See also MGI.

Green, E.L. 1954. The genetics of a new hair deficiency, furless, in the house mouse. J. Hered. 45: 115-118.
See also MGI.

Green, E.L., and M.C.Green. 1942. The development of three manifestations of the short ear gene in the mouse. J. Morphol. 70: 1-19.
See also MGI.

Green, E.L., and S.J. Mann. 1961. Opossum, a semi-dominant lethal mutation affecting hair and other characteristics of mice. J. Hered. 52: 223-227.
See also MGI.

Green, M.C. 1951. Further morphological effects of the short ear gene in the house mouse. J. Morphol. 88: 1-22.
See also MGI.

Green, M.C. 1955. Luxoid, a new hereditary leg and foot abnormality in the house mouse. J. Hered. 46: 91-99.
See also MGI.

Green, M.C. 1958. Effects of the short ear gene in the mouse on cartilage formation in healing bone fractures. J. Exp. Zool. 137: 75-88.
See also MGI.

Green, M.C. 1960. Mouse News Letter 23: 34.
See also MGI.

Green, M.C. 1961a. Himalayan, a new allele of albino in the mouse. J. Hered. 52: 73-75.
See also MGI.

Green, M.C. 1961b. The position of luxoid in linkage group II of the mouse. J. Hered. 52: 297-300.
See also MGI.

Green, M.C. 1962. Mouse News Letter 26: 34.
See also MGI.

Green, M.C. 1963. Methods for testing linkage, p. 56-82. In W.J. Burdette [ed.] Methodology in Mammalian Genetics. Holden-Day, San Francisco.

Green, M.C. 1964a. Mouse News Letter 30: 32.
See also MGI.

Green, M.C. 1964b. Mouse News Letter 31: 27.
See also MGI.

Green, M.C. 1965. Mouse News Letter 32: 46.

Green, M.C., and S.C. Fox. 1965. Mouse News Letter 32: 46.
See also MGI.

Green, M.C., and R.L. Sidman. 1962. Tottering, a neuromuscular mutation in the mouse and its linkage with oligosyndactylism. J. Hered. 53: 233-237.
See also MGI.

Green, M.C., G.D. Snell, and P.W. Lane. 1963. Linkage group XVIII of the mouse. J. Hered. 54: 245-247.
See also MGI.

Grewal, M.S. 1962a. The development of an inherited tooth defect in the mouse. J. Embryol. Exp. Morphol. 10: 202-211.
See also MGI.

Grewal, M.S. 1962b. A sex-linked anaemia in the mouse. Genet. Res. 3: 238-247.

Grobman, A.B., and D.R. Charles. 1947. Mutant white mice. A new dominant autosomal mutant affecting coat color in Mus musculus. J. Hered. 38: 381-384.
See also MGI.

Grüneberg, H. 1935a. A three-factor linkage experiment in the mouse. J. Genet. 31: 157-162.
See also MGI.

Grüneberg, H. 1935b. A new sub-lethal colour mutation in the house mouse. Proc. Roy. Soc. B 118: 321-342.
See also MGI.

Grüneberg, H. 1936. Further linkage data on the albino chromosome of the house mouse. J. Genet. 33: 255-265.
See also MGI.

Grüneberg, H. 1942a. The anemia of flexed-tail mice. II. Siderocytes. J. Genet. 44: 246-271.
See also MGI.

Grüneberg, H. 1942b. Inherited macrocytic anaemias in the house mouse. II. Dominance relationships. J. Genet. 43: 285-293.
See also MGI.

Grüneberg, H. 1943a. Congenital hydrocephalus in the mouse, a case of spurious pleiotropism. J. Genet. 45: 1-21.
See also MGI.

Grüneberg, H. 1943b. Two new mutant genes in the house mouse. J. Genet. 45: 22-28.
See also MGI.

Grüneberg, H. 1948. Some observations on the microphthalmia gene in the mouse. J. Genet. 49: 1-13.
See also MGI.

Grüneberg, H. 1950. Some observations on the skeleton of the mouse. II. Undulated and its "modifiers." J. Genet. 50: 142-173.
See also MGI.

Grüneberg, H. 1952. The Genetics of the Mouse, 2nd ed. Nijhoff, The Hague. 650 p.
See also MGI.

Grüneberg, H. 1953a. Genetical studies on the skeleton of the mouse. VI. Danforth's short-tail. J. Genet. 51: 317-326.
See also MGI.

Grüneberg, H. 1953b. Genetical studies on the skeleton of the mouse. VII. Congenital hydrocephalus. J. Genet. 51: 327-358.
See also MGI.

Grüneberg, H. 1953c. The relations of microphthalmia and white in the mouse. J. Genet. 51: 359-362.
See also MGI.

Grüneberg, H. 1954a. Genetical studies on the skeleton of the mouse. VIII. Curly-tail. J. Genet. 52: 52-67.
See also MGI.

Grüneberg, H. 1954b. Genetical studies on the skeleton of the mouse. XII. The development of undulated. J. Genet. 52: 441-455.
See also MGI.

Grüneberg, H. 1955a. Genetical studies on the skeleton of the mouse. XVI. Tail-kinks. J. Genet. 53: 536-550.
See also MGI.

Grüneberg, H. 1955b. Genetical studies on the skeleton of the mouse. XVII. Bent-tail. J. Genet. 53: 551-562.
See also MGI.

Grüneberg, H. 1956. Genetical studies on the skeleton of the mouse. XVIII. Three genes for syndactylism. J. Genet. 54: 113-145.
See also MGI.

Grüneberg, H. 1957. Genetical studies on the skeleton of the mouse. XIX. Vestigial tail. J. Genet. 55: 181-194.
See also MGI.

Grüneberg, H. 1958a. Genetical studies on the skeleton of the mouse. XXII. The development of Danforth's short-tail. J. Embryol. Exp. Morphol. 6: 124-148.
See also MGI.

Grüneberg, H. 1958b. Genetical studies on the skeleton of the mouse. XXIII. The development of brachyury and anury. J. Embryol. Exp. Morphol. 6: 424-443.
See also MGI.

Grüneberg, H. 1960. Genetical studies on the skeleton of the mouse. XXV. The development of syndactylism. Genet. Res. 1: 196-213.
See also MGI.

Grüneberg, H. 1961a. Genetical studies on the skeleton of the mouse. XXVII. The development of oligosyndactylism. Genet. Res. 2: 33-42.
See also MGI.

Grüneberg, H. 1961b. Genetical studies on the skeleton of the mouse. XXIX. Pudgy. Genet. Res. 2: 384-393.
See also MGI.

Grüneberg, H. 1962. Genetical studies on the skeleton of the mouse. XXXII. The development of shaker with syndactylism. Genet. Res. 3: 157-166.
See also MGI.

Grüneberg, H. 1963. The Pathology of Development. Wiley, New York. 309 p.

Grüneberg, H., J.B. Burnett, and G.D. Snell. 1941. The origin of jerker, a new gene mutation of the house mouse, and linkage studies made with it. Proc. Nat. Acad. Sci. 27: 562-565.
See also MGI.

Grüneberg, H., and G.M. Truslove. 1960. Two closely linked genes in the mouse. Genet. Res. 1: 69-90.
See also MGI.

Hamburgh, M. 1963. Analysis of the postnatal development of "reeler," a neurological mutation in mice. A study in developmental genetics. Develop. Biol. 8: 165-185.
See also PubMed.

Harman, P.J. 1950. Polycytic alterations in the white matter of the brain of the "jittery" mouse. Anat. Rec. 106: 304. (Abstr.)
See also MGI.

Harman, P.J. 1954. Genetically controlled demyelination in the mammalian central nervous system. Ann. N.Y. Acad. Sci. 58: 546-550.
See also MGI.

Henderson, N.S. 1965. Isozymes of isocitrate dehydrogenase: subunit structure and intracellular location. J. Exp. Zool. 158: 263-273.
See also MGI.

Herbertson, B.M., and M.E. Wallace. 1964. Chylous ascites in newborn mice. J. Med. Genet. 1: 10-23.
See also MGI.

Hertwig, P. 1939. Zwei subletale recessive Mutationen in der Nachkommenschaft von röntgenbestrahlten Mäusen. Erbarzt 6: 41-43.
See also MGI.

Hertwig, P. 1942. Neue Mutationen und Koppelungsgruppen bei der Hausmaus. Z. Indukt. Abstamm. Vereb. 80: 220-246.
See also MGI.

Hertwig, P. 1944. Die Genese der Hirn- und Gehöroganmissbildungen bei röntgenmutierten Kreiseler-Mäusen. Z. Mensch. Vereb. Konst. 28: 327-354.

Herzenberg, L.A. 1964. A chromosome region for gamma_2a and beta_2a globulin H chain isoantigens in the mouse. Cold Spring Harbor Symp. Quant. Biol. 29: 455-462.
See also MGI.

Herzenberg, L.A., R.I. Mishell, and L.A. Herzenberg. 1963a. Gamma-globulin isoantigens (allotypes) in the house mouse, p. 196. In S.J. Geerts [ed.] Proc. XI Int. Congr. Genet. Vol. 1. Pergamon Press, New York. (Abstr.)
See also MGI.

Herzenberg, L.A., D.K. Tachibana, L.A. Herzenberg, and L.T. Rosenberg. 1963b. A gene locus concerned with hemolytic complement in Mus musculus. Genetics 48: 711-714.
See also MGI.

Herzenberg, L.A., N.L. Warner, and L.A. Herzenberg. 1965. Immunoglobulin isoantigens (allotypes) in the mouse. I. Genetics and cross-reactions of the 7S _γ2a-isoantigens controlled by alleles at the Ig-1 locus. J. Exp. Med. 121: 415-438.
See also PubMed.

Heston, W.E. 1941. Relationship between susceptibility to induced pulmonary tumors and certain known genes in mice. J. Nat. Cancer Inst. 2: 127-132.

Heston, W.E. 1951. The "vestigial tail" mouse; a new recessive mutation. J. Hered. 42: 71-74.
See also PubMed.

Heston, W.E., H.A. Hoffman, and M. Rechcigl. 1965. Genetic analysis of liver catalase activity in two substrains of C57BL mice. Genet. Res. 6: 387-397.
See also PubMed.

Heston, W.E., and M. Rechcigl. 1964. Genetic analysis of liver catalase activity in C57BL mice. Proc. Amer. Ass. Cancer Res. 5: 26 (Abstr.)

Hirsch, M.S. 1962. Studies on the response of osteopetrotic bone explants to parathyroid explants in vitro. Bull. Johns Hopkins Hosp. 110: 257-264.
See also PubMed.

Hoecker, G., A. Martinez, S. Markovic, and O. Pizzaro. 1954. Agitans, a new mutation in the house mouse with neurological effects. J. Hered. 45: 10-14.
See also MGI.

Hollander, W.F. 1959. Mouse News Letter 20: 34-35.

Hollander, W.F. 1960. Genetics in relation to reproductive physiology in mammals. J. Cell. Comp. Physiol. 56: 61-72.
See also MGI.

Hollander, W.F. 1964. Mouse News Letter 30: 29.
See also MGI.

Hollander, W.F., J.H.D. Bryan, and J.W. Gowen. 1960. Pleiotropic effects of a mutant at the p locus from X-irradiated mice. Genetics 45: 413-418.
See also MGI.

Hollander, W.F., and J.W. Gowen. 1956. An extreme non-agouti mutant in the mouse. J. Hered. 47: 221-224.
See also MGI.

Hollander, W.F., and J.W. Gowen. 1959. A single-gene antagonism between mother and fetus in the mouse. Proc. Soc. Exp. Biol. Med. 101: 425-428.
See also MGI.

Hollander, W.F., and L.C. Strong. 1951. Pintail, a dominant mutation linked with brown in the house mouse. J. Hered. 42: 179-182.
See also MGI.

Holman, S.P. 1951. The hook-tailed mouse. J. Hered. 42: 305-306.
See also MGI.

Holt, S.B. 1945. A polydactyl gene in mice capable of nearly regular manifestation. Ann. Eugen. 12: 220-249.
See also MGI.

Howard, A. 1940. "Rhino," an allele of hairless in the house mouse. J. Hered. 31: 467-470.
See also MGI.

Hulse, E.V., M.F. Lyon, and R. Meredith. 1965. Mouse News Letter 32: 38.
See also MGI.

Hummel, K.P. 1958. The inheritance and expression of disorganization, an unusual mutation in the mouse. J. Exp. Zool. 137: 389-423.
See also MGI.

Hummel, K.P. 1959. Developmental anomalies in mice resulting from action of the gene, disorganization, a semi-dominant lethal. Pediatrics 23: 212-221.
See also MGI.

Hummel, K.P., and D.B. Chapman. 1959. Visceral inversion and associated anomalies in the mouse. J. Hered. 50: 9-13.
See also MGI.

Hummel, K.P., and D.B. Chapman. 1963. Mouse News Letter 28: 32.

Hunsicker, P.R. 1960. Mouse News Letter 28: 58.
See also MGI.

Hunt, H.R., R. Mixter, and D. Permar. 1933. Flexed tail in the mouse, Mus musculus. Genetics 18: 335-366.
See also MGI.

Hutton, J.J., J. Bishop, R. Schweet, and E.S. Russell. 1962a. Hemoglobin inheritance in inbred mouse strains. I. Structural differences. Proc. Nat. Acad. Sci. 48: 1505-1513.
See also PubMed.

Hutton, J.J., J. Bishop, R. Schweet, and E.S. Russell. 1962b. Hemoglobin inheritance in inbred mouse strains. II. Genetic studies. Proc. Nat. Acad. Sci. 48: 1718-1724.
See also MGI.

Hutton, J.J., R.S. Schweet, H.G. Wolfe, and E.S. Russell. 1964. Hemoglobin solubility an α-chain structure in crosses between two inbred mouse strains. Science 143: 252-253.
See also PubMed.

Ingalls, A.M., M.M. Dickie, and G.D. Snell 1950. Obese, a new mutation in the house mouse. J. Hered. 41: 317-318.
See also MGI.

Isaacson, J.H., and B.M. Cattanach. 1962. Mouse News Letter 27: 31.
See also MGI.

Jarrett, A., and R.I. Spearman. 1957. The keratin defect and hair-cycle of a new mutant (matted) in the house-mouse. J. Embryol. Exp. Morphol. 5: 103-110.
See also MGI.

Joe, M., J.M. Teasdale, and J.R. Miller. 1962. A new mutation (sph) causing neonatal jaundice in the house mouse. Can J. Genet. Cytol. 4: 219-225.
See also MGI.

Johnson, P.L. 1926. An anatomical study of abnormal jaws in the progeny of X-rayed mice. Amer. J. Anat. 38: 281-317.
See also MGI.

Kadam, K.M. 1962. Genetical studies on the skeleton of the mouse. XXXI. The muscular anatomy of syndactylism and oligosyndactylism. Genet. Res. 3: 139-156.
See also MGI.

Kamenoff, R.J. 1935. Effects of the flexed-tailed gene on the development of the house mouse. J. Morphol. 58: 117-155.
See also MGI.

Kantoch, M., A. Warwick, and F.B. Bang. 1963. The cellular nature of genetic susceptibility to a virus. J. Exp. Med. 117: 781-798.
See also MGI.

Keeler, C.E. 1924. The inheritance of a retinal abnormality in white mice. Proc. Nat. Acad. Sci. 10: 329-333.
See also MGI.

Keeler, C.E. 1927a. Sur l'origne de caractère "sans bâtonnets" chez la souris domestique. Bull. Soc. Zool. France 52: 520-521.

Keeler, C.E. 1927b. Rodless retina, an ophthalmic mutation in the house mouse, Mus musculus. J. Exp. Zool. 46: 355-407.

Keeler, C.E. 1928. Blind mice. J. Exp. Zool. 51: 495-508.

Keeler, C.E. 1930. Hereditary Blindness in the House Mouse with Special Reference to its Linkage Relationships. Howe Lab. Ophthalmol. Bull. No. 2. 11 p.

Keeler, C.E. 1931. The Laboratory Mouse. Harvard Univ. Press, Cambridge, Mass. 81 p.
See also MGI.

Keeler, C.E. 1935. A second rexoid coat character in the house mouse. J. Hered. 26: 189-191.
See also MGI.

Kelly, E.M. 1953. Mouse News Letter 8 (Suppl.): 15.
See also MGI.

Kelly, E.M. 1955. Mouse News Letter 12: 48.
See also MGI.

Kelly, E.M. 1957. Mouse News Letter. 16: 36.
See also MGI.

Kelly, E.M. 1958. Mouse News Letter 19: 37.
See also MGI.

Kelly, E.M., and J.W. Bangham. 1955. Mouse News Letter 12: 47.
See also MGI.

Kelton, D.E. 1965. Mouse News Letter 32: 60.
See also MGI.

Kelton, D.E., and H. Rauch. 1962. Myelination and myelin degeneration in the central nervous system of dilute-lethal mice. Exp. Neurol. 6: 252-262.
See also PubMed.

Kelton, D.E., and V. Smith. 1964. Gaping, a new open-eyelid mutation in the house mouse. Genetics 50: 261-262. (Abstr.)
See also MGI.

Kelus, A., and J.K. Moor-Jankowski. 1961. An iso-antigen (_γB^A) of mouse γ-globulin present in inbred strains. Nature 191: 1405-1406.
See also PubMed.

Kidwell, J.F., J.W. Gowen, and J. Stadler. 1961. Pugnose-a recessive mutation in linkage group 3 of mice. J. Hered. 52: 145-148.
See also MGI.

King, J.W.B. 1950. Pygmy, a dwarfing gene in the house mouse. J. Hered. 41: 249-252.
See also MGI.

King, J.W.B. 1955. Observations on the mutant "pygmy" in the house mouse. J. Genet. 53: 487-497.
See also MGI.

King, J.W.B. 1956. Linkage group XIV of the house mouse. Nature 178: 1126-1127.
See also MGI.

King, L.S. 1936. Hereditary defects of the corpus callosum in the mouse, Mus musculus. J. Comp. Neurol. 64: 337-363.
See also MGI.

King, L.S., and C.E. Keeler. 1932. Absence of corpus callosum, a hereditary brain anomaly of the house mouse. Preliminary report. Proc. Nat. Acad. Sci. 18: 525-528.
See also MGI.

Kobozieff, N., and N.A. Pomriaskinsky-Kobozieff. 1962. Hémimélie chez la souris. Rec. Méd. Vét. 138: 671-686.

Kocher, W. 1960a. Untersuchen zur Genetik und Pathologie der Entwicklung von 8 Labyrinthmutanten (deaf-waltzer-shaker-Mutanten) der Maus (Mus musculus). Z. Vererb. 91: 114-140.
See also MGI.

Kocher, W. 1960b. Untersuchungen zur Genetik und Pathologie der Entwicklung spateinsetzender hereditarer Taubheit bei der Maus (Mus musculus). Arch. Ohr. Nas. Kehlkophheilk. 177: 108-145.
See also MGI.

Konyukhov, B.V., and D.M. Glukharev. 1962. The genetic and morphological characteristics of microphthalmic mice (blind mutants) [English transl.]. Bull Exp. Biol. Med. 52: 1437-1440.
See also MGI.

Konyukhov, B.V., O.G. Stroeva, M.V. Sazhina, and T.A. Lipgart. 1963. Retinal injury as a cause of microphthalmia in mice of the ocular retardation mutant line [in Russian, English summary]. Arkh. Anat. Gistol. Embriol. 44: 36-43.

Kreitner, P.C. 1957. Linkage studies in a new black-eyed white mutation in the house mouse (not W). J. Hered. 48: 300-304.
See also MGI.

Kuharcik, A.M., and P.F. Forsthoefel. 1963. A study of the anemia in Strong's luxoid mutant. J. Morphol. 112: 13-21.

Kunze, H.G. 1954. Die Erythropoese bei einer erblichen Anämie röntgenmutierter Mäusse. Folia Haematol. 72: 391-436.

Landauer, W. 1952. Brachypodism, a recessive mutation of house-mice. J. Hered. 43: 293-298.
See also MGI.

Lane, P.W. 1958. Mouse News Letter 19: 25.
See also MGI.

Lane, P.W. 1960a. Mouse News Letter 22: 35.
See also MGI.

Lane, P.W. 1960b. Mouse News Letter 23: 36.
See also MGI.

Lane, P.W. 1961. Mouse News Letter 25: 38.

Lane, P.W. 1962a. Mouse News Letter 26: 35.

Lane, P.W. 1962b. Mouse News Letter 27: 38.
See also MGI.

Lane, P.W. 1963. Whirler mice, a recessive behavior mutation in linkage group VIII. J. Hered. 54: 263-266.
See also MGI.

Lane, P.W. 1964. Mouse News Letter 30: 32.
See also MGI.

Lane, P.W. 1965. Mouse News Letter 32: 47.
See also MGI.

Lane, P.W., 1966. Association of megacolon with two recessive spotting genes in the mouse. J. Hered. 57: 29-31.
See also MGI.

Lane, P.W., and M.M. Dickie. 1961. Linkage of wabbler-lethal and hairless in the mouse. J. Hered. 52: 159-160.
See also MGI.

Lane, P.W., and M.C. Green. 1960. Mahogany, a recessive color mutation in linkage group V of the mouse. J. Hered. 51: 228-230.
See also MGI.

Lane, P.W., and M.C. Green. 1962. Mouse News Letter 27: 38.
See also MGI.

Larsen, M.M. 1961. Mouse News Letter 24: 60.

Larsen, M.M. 1963. Mouse News Letter 29: 73.

Larsen, M.M. 1964. Mouse News Letter 30: 47.
See also MGI.

Law, L.W., A.G. Morrow, and E.M. Greenspan. 1952. Inheritance of low liver glucuronidase activity in the mouse. J. Nat. Cancer Inst. 12: 909-916.

Lebedinsky, N.G., and A. Dauwart. 1927. Atrichosis und ihre Vererbung bei der albinotischen Hausmaus. Biol. Zentralbl. 47: 748-752.
See also MGI.

Levan, A., .C. Hsu, and H.F. Stich. 1962. The idiogram of the mouse. Hereditas 48: 677-687.

Lieberman, R., and S. Dray. 1964. Five allelic genes at the Asa locus which control γ-globulin allotypic specificities in mice. J. Immunol. 93: 584-594.
See also PubMed.

Lieberman, R., S. Dray, and M. Potter. 1965. Linkage in control of allotypic specificities on two different gamma-G-immunoglobulins. Science. 148: 640-642.
See also PubMed.

Lindenmann, J. 1964. Inheritance of resistance to influenza virus in mice. Proc. Soc. Exp. Biol. Med. 116: 506-509.
See also PubMed.

Little, C.C., and H.J. Bagg. 1923. The occurrence of two heritable types of abnormality among the descendants of X-rayed mice. Amer. J. Roentgenol. 10: 975-989.
See also MGI.

Little, C.C., and H.J. Bagg. 1924. The occurrence of four inheritable morphological variations in mice and their possible relation to treatment with X-rays. J. Exp. Zool. 41: 45-91.
See also MGI.

Little, C.C., and A.M. Cloudman. 1937. The occurrence of a dominant spotting mutation in the house mouse. Proc. Nat. Acad. Sci. 23: 535-537.
See also MGI.

Loosli, R. 1963. Tanoid - a new agouti mutant in the mouse. J. Hered. 54: 26-29.
See also MGI.

Lord, E.M., and W.H. Gates. 1929. Shaker, a new mutation of the house mouse. Amer. Natur. 63: 435-442.
See also MGI.

Lynch, C.J. 1921. Short ears, an autosomal mutation in the house mouse. Amer. Natur. 55: 421-426.
See also MGI.

Lyon, M.F. 1953. Absence of otoliths in the mouse: an effect of the pallid mutant. J. Genet. 51: 638-650.
See also MGI.

Lyon, M.F. 1955a. The developmental origin of hereditary absences of otoliths in mice. J. Embryol. Exp. Morphol. 3: 230-241.
See also MGI.

Lyon, M.F. 1955b. Ataxia - a new recessive mutant of the house mouse. J. Hered. 46: 77-80.
See also MGI.

Lyon, M.F. 1956. Hereditary hair loss in the tufted mutant of the house mouse. J. Hered. 47: 101-103.
See also MGI.

Lyon, M.F. 1958. Twirler: a mutant affecting the inner ear of the house mouse. J. Embryol. Exp. Morphol. 6: 105-116.
See also MGI.

Lyon, M.F. 1959. A new dominant T-allele in the house mouse. J. Hered. 50: 140-142.
See also MGI.

Lyon, M.F. 1960. A further mutation of the mottled type in the house mouse. Genet. Res. 2: 92-95.
See also MGI.

Lyon, M.F. 1961a. Linkage relations and some pleiotropic effects of the dreher mutant of the house mouse. Genet. Res. 2: 92-95.
See also MGI.

Lyon, M.F. 1961b. Mouse News Letter 24: 34.

Lyon, M.F. 1963a. Attempts to test the inactive-X theory of dosage compensation in mammals. Genet. Res. 4: 93-103.
See also MGI.

Lyon, M.F. 1963b. Genetics of the mouse, p. 199-234. In W. Lane-Petter [ed.] Animals for Research. Academic Press, London and New York.

Lyon, M.F. 1965. Mouse News Letter 32: 39.

Lyon, M.F., E.V. Hulse, and C.E. Rowe. 1965. Foam-cell reticulosis of mice: an inherited condition resembling Gaucher's and Niemann-Pick diseases. J. Med. Genet. 2: 99-106.
See also MGI.

Lyon, M.F., and R. Meredith. 1963. Mouse News Letter 28: 29.

Lyon, M.F., and R. Meredith. 1964. The nature of t-alleles in the mouse. Heredity 19: 301-330.
See also MGI.

Lyon, M.F., and R. Meredith. 1965. Mouse News Letter 32: 38.
See also MGI.

Lyon, M.F., and R.J.S. Phillips. 1959. Crossing-over in mice heterozygous for t-alleles. Heredity 13: 23-32.

Lyon, M.F., R.J.S. Phillips, and A.G. Searle. 1964a. The overall rates of dominant and recessive lethal and visible mutation induced by spermatogonial X-irradiation of mice. Genet. Res. 5: 448-467.
See also MGI.

Lyon, M.F., A.G. Searle, C.E. Ford, and S. Ohno. 1964b. A mouse translocation suppressing sex-linked variegation. Cytogenetics 3: 306-323.
See also PubMed.

MacArthur, J.W. 1944. Genetics of body size and related characters. Amer. Natur. 78: 142-157, 224-237.
See also MGI.

MacDowell, E.C. 1950. "Light" - a new mouse color. J. Hered. 41: 35-36.
See also MGI.

MacDowell, E.C., J.S. Potter, T. Laanes, and E.N. Ward. 1942. The manifold effects of the screw-tail mouse mutation. A remarkable example of "pleiotropy" in genetically uniform material. J. Hered. 33: 439-449.
See also MGI.

Mackensen, J.A. 1960. "Open eyelids" in newborn mice. J. Hered. 51: 188-190.
See also MGI.

Mackensen, J.A. 1962. Mouse News Letter 27: 38.
See also MGI.

Mackensen, J.A., and L.C. Stevens. 1960. Rib fusions, a new mutation in the mouse. J. Hered. 51: 264-268.
See also MGI.

Maddux, S.C. 1964. Mouse News Letter 31: 41.
See also MGI.

Major, M.H. 1955. Mouse News Letter 12: 47.
See also MGI.

Major, M.H., and M.S. Hawkins. 1958. Mouse News Letter 19: 37.
See also MGI.

Mallyon, S.A. 1951. A pronounced sex difference in recombination values in the sixth chromosome of the house mouse. Nature 168: 118-119.
See also PubMed.

Mann, S.J. 1963. The phenogenetics of hair mutants in the house mouse: opossum and ragged. Genet. Res. 4: 1-11.
See also MGI.

Mann, S.J. 1964. The hair of the fuzzy mouse. J. Hered. 55: 121-123.
See also MGI.

Mann, S.J., and W.E. Straile. 1961. New observations on hair loss in the hairless mouse. Anat. Rec. 140: 97-102.

Margolis, F.L. 1965. Reduced δ-aminolevulinate dehydratase (ALD) activity in a mutant mouse anemia. Fed. Proc. 24: 469. (Abstr.)

Markert, C.L. 1960. Biochemical embryology and genetics. In N. Kaliss [ed.] Symposium on Normal and Abnormal Differentiation and Development. Nat. Cancer Inst. Monogr. 2: 3-17.
See also MGI.

Markert, C.L., and W.K. Silvers. 1956. The effects of genotype and cell environment on melanoblast differentiation in the house mouse. Genetics 41: 429-450.
See also MGI.

Markert, C.L., and W. K. Silvers. 1959. Effects of genotype and cellular environment on melanocytes morphology, p. 241-248. In M. Gordon [ed.] Pigment Cell Biology. Academic Press, New York.

Martinez, A., and J.L. Sirlin. 1955. Neurohistology of the agitans mouse. J. Comp. Neurol. 103: 131-137.
See also MGI.

Mather, K. 1951. The Measurement of Linkage in Heredity, 2nd ed. Wiley, New York. 149 p.

Mather, K., and S.B. North. 1940. Umbrous: a case of dominance modification in mice. J. Genet. 40: 229-241.
See also MGI.

Matter, H. 1957. Die formale Genese einer vererbten Eirbelsäulenmissbildung am Beispiel der Mutante Crooked-tail der Maus. Rev. Suisse Zool. 64: 1-38.
See also MGI.

Mauer, T. 1961. The effect of vitamin A in hyperkeratotic mouse mutants. J. Exp. Zool. 146: 181-207.
See also MGI.

Mayer, J. 1960. Genetic factors in obesity. Bull. N.Y. Acad. Med. 36: 323-343.

Mayer, T.C. 1965. The development of piebald spotting in mice. Develop. Biol. 11: 319-334.
See also MGI.

Mayer, T.C., and E. Maltby. 1964. An experimental investigation of pattern development in lethal spotting and belted mouse embryos. Develop. Biol. 9: 269-286.
See also MGI.

McNutt, W. 1962. Urinary amino acid excretion in quivering mice (qvqv). Anat. Rec. 142: 257. (Abstr.)
See also MGI.

Meier, H., and W.G. Hoag. 1962. The neuropathology of "reeler," a neuromuscular mutation in mice. J. Neuropathol. Exp. Neurol. 21: 649-654.

Menner, K. 1957. Die postnatale Gonadenentwicklung bei Mäusen, die an einer angeborenen Anämie leiden. Wiss. Z. Martin-Luther-Univ. 6: 335-344.

Meredith, R. 1964. Mouse News Letter 31: 25.
See also MGI.

Meredith, R. 1965. Mouse News Letter 32: 39.
See also MGI.

Michelson, A.M., E.S. Russell, and P.J. Harman. 1955. Dystrophia muscularis: a hereditary primary myopathy in the house mouse. Proc. Nat. Acad. Sci. 41: 1079-1084.
See also MGI.

Michie, D. 1955a. Genetical studies with "vestigial tail" mice. I and II. J. Genet. 53: 270-284.
See also MGI.

Michie, D. 1955b. "Affinity." Proc. Roy. Soc. B 144: 241-259.
See also PubMed.

Michie, D., and M.E. Wallace. 1953. Affinity: a new genetic phenomenon in the house mouse; evidence from distant crosses. Nature 171: 26.
See also PubMed.

Mikaelian, D.O., and R.J. Ruben. 1964. Hearing degeneration in shaker-1 mouse. Arch. Otolaryngol. 80: 418-430.
See also MGI.

Milaire, J. 1962. Détection histochimie de modifications des ébauches dans les membres en formation chez la souris oligosyndactyl. Bull. Acad. Roy. Belgique 1962. p. 505-528.

Miller, D.S. 1963. Coat color and behavior mutations in inbred mice under chronic low-level γ-irradiation. Radiat. Res. 19: 184-185.
See also MGI.

Miller, D.S., and M.Z. Potas. 1955. Cordovan, a new allele of black and brown color in the mouse. J. Hered. 46: 293-296.
See also MGI.

Miller, J.R. 1964. Mouse News Letter 30: 16.
See also MGI.

Mintz, B. and E.S. Russell. 1957. Gene-induced embryological modifications of primordial germ cells in the mouse. J. Exp. Zool. 134: 207-237.
See also MGI.

Mishell, R.K., and J.L. Fahey. 1964. Molecular and submolecular localization of the two isoantigens of mouse immunoglobulins. Science 143: 1440-1442.
See also PubMed.

Montagna, W., H.B. Chase, and H.P. Melaragno. 1952. The skin of hairless mice. I. The formation of cysts and the distribution of lipids. J. Invest. Dermatol. 19: 83-94.
See also MGI.

Morgan, W.C. 1950. A new tail-short mutation in the mouse whose lethal effects are conditioned by the residual genotypes. J. Hered. 41: 208-215.
See also MGI.

Morgan, W.C. 1954. A new crooked tail mutation involving distinctive pleiotropism. J. Genet. 52: 354-373.
See also MGI.

Morton, J.R. 1962. Starch-gel electrophoresis of mouse haemoglobina. Nature 194: 383-384.
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Mufson, M.A., and A. Starr. 1958. Abnormal myelin and leukopenia in the wabbler-lethal mouse. J. Hered. 49: 233-237.

Müller, G. 1950. Eine entwicklungsgeschichtliche Untersuchung über das erbliche Kolobom mit Mikrophthalmus bei der Hausmaus. Z. Mikroshop.-Anat. Forsch. 56: 520-558.

Müller, G. 1951. Die embryonale Entwicklung eines sich rezessiv vererbenden Merkmals. (Kolobom bei der Hausmaus). Wiss. Z. Martin-Luther-Univ. 1: 27-43.

Murphy, E.D., and E.S. Russell. 1963. Ovarian tumorigenesis following genic deletion of germ cells in hybrid mice. Acta. Un. Int. Contra Cancrum 19: 779-782.
See also PubMed.

Murray, J.M. 1933. "Leaden," a recent color mutation in the house mouse. Amer. Natur. 67: 278-283.
See also MGI.

Murray, J.M., and G.D. Snell. 1945. Belted, a new sixth chromosome mutation in the mouse. J. Hered. 36: 266-268.
See also MGI.

Nakamura, A., H. Sakamoto, and K. Moriwaki. 1963. Genetical studies of post-axial polydactyly in the house mouse. Ann. Rep. Nat. Inst. Genet. Jap. (1962) 13: 31.

Nash, D.J. 1964. Mouse News Letter 30: 53-54.
See also MGI.

Nash, D.J., E. Kent, M.M. Dickie, and E.S. Russell. 1964. The inheritance of "mick" and new anemia in the house mouse. Amer. Zool. 4: 404-405.

Nasrat, G.E. 1956. Estimation of the recombination fraction between the two linked genes Re and sh-2 in the house mouse when the female is the heterozygous parent. Proc. Zool. Soc. (Bengal) 9: 85-87.
See also MGI.

Nolte, D.J. 1957. Mouse News Letter 17: 100.

Old, L.J., E.A. Boyse, and E. Stockert. 1963. Antigenic properties of experimental leukemias. I. Serological studies in vitro with spontaneous and radiation-induced leukemias. J. Nat. Cancer Inst. 31: 977-995.

Paget, O.E. 1953. Cataracta hereditaria subcapsularis: ein neues, dominantes Allel bei der Hausmaus. Z. Induckt. Abstamm. Vererb. 85: 238-244.
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Paget, O.E., and M. Baumgartner-Gamauf, 1961. Histologische Untersuchen an einer dominant erblichen Form einer Cataract bei der Hausmaus. Zool. Anz. 166: 55-69.

Pai, A.C. 1965. Developmental genetics of a lethal mutation, muscular dysgenesis (mdg) in the mouse. I and II. Develop. Biol. 11: 82-109.
See also MGI.

Paigen, K. 1961a. The genetic control of enzyme activity during differentiation. Proc. Natl. Acad. Sci. 47: 1641-1649.
See also MGI.

Paigen, K. 1961b. The effect of mutation on the intracellular location of beta-glucuronidase. Exp. Cell Res. 25: 286-301.
See also PubMed.

Paigen, K. 1964. The genetic control of enzyme realization during differentiation, p. 181-190. In: Second Int. Conf. Congen. Malformations. Int. Med. Congr. Ltd., New York.

Paigen, K., and W.K. Noell. 1961. Two linked genes showing a similar timing of expression in mice. Nature 190: 148-150.
See also MGI.

Parsons, P.A. 1958a. A balanced four-point linkage experiment for a linkage group XIII of the house mouse. Heredity 12: 77-95.
See also MGI.

Parsons, P.A. 1958b. Additional three-point data for linkage group V of the mouse. Heredity 12: 357-362.
See also MGI.

Parsons, P.A. 1959. Possible affinity between linkage groups V and XIII of the house mouse. Genetica 29: 304-311.

Pelzer, C.F. 1965. Genetic control of erthrocytic esterase forms in Mus musculus. Proc. Nat. Acad. Sci. 50: 112-116.
See also MGI.

Petras, M.L. 1963. Genetic control of a serum esterase component in Mus musculus. Proc. Nat. Acad. Sci. 50: 112-116.
See also MGI.

Phillips, R.J.S. 1954. Jimpy, a new totally sex-linked gene in the house mouse. Z.Induckt. Abstamm. Vererb. 86: 322-326.
See also MGI.

Phillips, R.J.S. 1956. The linkages of congenital hydrocephalus in the house mouse. J. Hered. 47: 302-304.
See also MGI.

Phillips, R.J.S. 1960a. "Lurcher," a new gene in linkage group XI of the house mouse. J. Genet. 57: 35-42.
See also MGI.

Phillips, R.J.S. 1960b. Mouse News Letter 23: 29-30.
See also MGI.

Phillips, R.J.S. 1961. "Dappled," a new allele at the mottled locus in the house mouse. Genet. Res. 2: 290-295.
See also MGI.

Phillips, R.J.S. 1962. Mouse News Letter 27: 34.
See also MGI.

Phillips, R.J.S. 1963a. Mouse News Letter 29: 37-38.

Phillips, R.J.S. 1963b. Striated, a new sex-linked gene in the house mouse. Genet. Res. 4: 151-153.
See also MGI.

Pierro, L.J. 1963a. Effects of the Light mutation of mouse coat color on eye pigmentation. J. Exp. Zool. 153: 81-87.
See also MGI.

Pierro, L.J. 1963b. Pigment granule formation in slate, a coat color mutant in the mouse. Anat. Rec. 146: 365-372.
See also PubMed.

Pierro, L.J., and H.B. Chase. 1963. Slate - a new coat color mutant in the mouse. J. Hered. 54: 47-50.
See also MGI.

Pierro, L.J., and H.B. Chase. 1965. Temporary hair loss assocaited with the slate mutation of coat color in the mouse. Nature 205: 579-580.
See also MGI.

Pizarro, O. 1957. Mouse News Letter 17: 96.
See also MGI.

Popp, R.A. 1962a. Studies on the mouse hemoglobin loci. II, III, IV. J. Hered. 53: 73-80.
See also MGI.

Popp, R.A. 1962b. Studies on the mouse hemoglobin loci. V, VI, VII. J. Hered. 53: 142-151.
See also MGI.

Popp, R.A. 1965a. Loci linkage of serum esterase patterns and oligosyndactylism. J. Hered. 56: 107-108.
See also MGI.

Popp, R.A. 1965b. Hemoglobin variants in mice. Fed Proc. 24: 1252-1257.
See also MGI.

Popp, R.A., and D.M. Popp. 1962. Inheritance of serum esterases having different electrophoretic patterns among inbred strains of mice. J. Hered. 53: 111-114.
See also MGI.

Popp, R.A., and W. St. Amand. 1960. Studies on the mouse hemoglobin locus. I. Identification of hemoglobin types and linkage of hemoglobin with albinism. J. Hered. 51: 141-144.
See also MGI.

Quevedo, W.C., Jr., and H.B. Chase. 1958. An analysis of the light mutation of coat color in mice. J. Morphol. 102: 329-345.
See also MGI.

Rabaud, E. 1914. Sur une anomalie héréditarie des membres postérieurs chez al souris. Compt. Rend. Soc. Biol. 77: 411-412.

Randelia, H.P., and L.D. Sanghvi. 1961. "Bare," a new hairless mutant in the mouse - genetics and histology. Genet. Res. 2: 283-289.
See also MGI.

Ranney, H.M., and S. Gluecksohn-Waelsch. 1955. Filter-paper electrophoresis of mouse haemoglobin: preliminary note. Ann. Hum. Genet. 19: 269-272.
See also PubMed.

Rauch, H., and M.T. Yost. 1963. Phenylalanine metabolism in dilute-lethal mice. Genetics 48: 1487-1495.
See also PubMed.

Rechcigl, M., and W.E. Heston. 1963. Tissue catalase activity in several C57BL substrains and in other strains of inbred mice. J. Nat. Cancer Inst. 30: 855-864.
See also MGI.

Reed, S.C. 1937. The inheritance and expression of fused, a new mutation in the house mouse. Genetics 22: 1-13.
See also MGI.

Roberts, E. 1931. A new mutation in the house mouse (Mus musculus). Science 74: 569.
See also MGI.

Robertson, G.G. 1942. An analysis of the development of homozygous yellow mouse embryos. J. Exp. Zool. 89: 197-231.

Robins, M.W. 1959. A mutation causing congenital clubfoot in the house mouse. J. Hered. 50: 188-192.
See also MGI.

Robinson, R. 1959. Sable and umbrous mice. Genetica 29: 319-326.
See also MGI.

Ruddle, F.H., and T.H. Roderick. 1965. The genetic control of three kidney esterases in C57BL/6J and RF/J mice. Genetics 51: 445-454.
See also PubMed.

Runner, M.N. 1959. Linkage of brachypodism. A new member of linkage group V of the house mouse. J. Hered. 50: 81-84.
See also MGI.

Russell, E.S. 1949a. A quantitative histological study of the pigment found in the coat color mutants of the house mouse. IV. The nature of the effects of genic substitution in five major allelic series. Genetics 34: 146-166.
See also MGI.

Russell, E.S. 1949b. Analysis of pleiotropism at the W-locus in the mouse: Relationship between the effects of W and W^v substitution on hair pigmentation and on erythrocytes. Genetics 34: 708-723.
See also MGI.

Russell, E.S., and E. Fekete. 1958. Analysis of W-series pleiotropism in the mouse: Effect of W^vW^v substitution on definitive germ cells and on ovarian tumorigenesis. J. Nat. Cancer Inst. 21: 365-381.
See also PubMed.

Russell, E.S., and P.S. Gerald. 1958. Inherited electrophoretic hemoglobin patterns among 20 inbred strains of mice. Science 128: 1569-1570.
See also MGI.

Russell, E.S., F. Lawson, and G. Schabtach. 1957. Evidence for a new allele at the W-locus of the mouse. J. Hered. 48: 119-123.
See also MGI.

Russell, E.S., L.M. Murray, E.M. Small, and W.K. Silvers. 1956. Development of embryonic mouse gonads transferred to the spleen: effects of transplantation combined with genotypic autonomy. J. Embryol. Exp. Morphol. 4: 347-357.

Russell, L.B. 1951. Mouse News Letter 5: 50.

Russell, L.B. 1960a. Mouse News Letter 22: 50.
See also MGI.

Russell, L.B. 1960b. Mouse News Letter 23: 58.
See also MGI.

Russell, L.B. 1961. Mouse News Letter 25: 64.
See also MGI.

Russell, L.B. 1963. Mouse News Letter 29: 73.
See also MGI.

Russell, L.B., and M.H. Major. 1956. A high rate of somatic reversion in the mouse. Genetics 41: 658. (Abstr.)

Russell, L.B., M.N.C. McDaniel, and F.N. Woodiel. 1963. Crossing-over within the A "locus" of the mouse. Genetics 48: 907. (Abstr.)

Russell, R.L., and D.L. Coleman. 1963. Genetic control of hepatic δ-aminolevulinate dehydratase in mice. Genetics 48: 1033-1039.
See also MGI.

Russell, W.L. 1947. Splotch, a new mutation in the house mouse, Mus musculus. Genetics 32: 102. (Abstr.)
See also MGI.

Russell, W.L. 1965. Evidence from mice concerning the nature of the mutation process. p. 257-264. In S.J. Geerts [ed.] Proc. XI Int. Congr. Genet. (The Hague, 1963) Vol. 2. Pergammon Press, New York.
See also MGI.

Russell, W.L., L.B. Russell, and J.S. Gower. 1959. Exceptional inheritance of a sex-linked gene in the mouse explained on the basis that the X/O sex-chromosome constitution is female. Proc. Nat. Acad. Sci. 45: 554-560.
See also MGI.

Sabin, A.B. 1952. Nature of inherited resistance to viruses affecting the nervous system. Proc. Natl. Acad. Sci. 38: 540-546.
See also MGI.

Sackler, A.M., A.S. Weltman, P. Steinglass, and S.D. Krauss. 1964. Endocrine differences between whirler and normal strains of female mice. Fed. Proc. 23: 252. (Abstr.)

Sarvella, P.A. 1954. Pearl, a new spontaneous coat and eye color mutation in the house mouse. J. Hered. 45: 19-20.
See also MGI.

Sarvella, P.A., and L.B. Russell. 1956. Steel, a new dominant gene in the house mouse. J. Hered. 47: 123-128.
See also MGI.

Saylors, C.L. 1961. Mouse News Letter 25: 64.

Schaible, R.H. 1956. Mouse News Letter 15: 29.
See also MGI.

Schaible, R.H. 1961. Mouse News Letter 24: 38.
See also MGI.

Schaible, R.H. 1963a. Mouse News Letter 28: 39.

Schaible, R.H. 1963b. Mouse News Letter 29: 48-49.
See also MGI.

Schaible, R.H. 1963c. Deveopmental genetics of spotting patterns in the mouse. Ph.D. Dissertation. Iowa State Univ., Ames. 225 p.
See also MGI.

Schaible, R.H., and J.W. Gowen. 1961. A new dwarf mouse. Genetics 46: 896. (Abstr.)

Scheufler, H. 1963. Erbliche Neugeborenengelbsucht - eine neue Mutante der Hausmaus. Z. Versuchstierk. 3: 27-29.

Schlesinger, M., E.A. Boyse, and L.J. Old. 1965. Thymus cells of radiation-chimeras: TL phenotype, sensitivity to guinea-pig serum, and origin from donor cells. Nature 206: 1119-1121.
See also PubMed.

Searle, A.G. 1952. A lethal allele of dilute in the house mouse. Heredity 6: 395-401.
See also MGI.

Searle, A.G. 1961. Tipsy, a new mutant in linkage group VII of the mouse. Genet. Res. 2: 122-126.
See also MGI.

Searle, A.G. 1964. The genetics and morphology of two "luxoid" mutants in the house mouse. Genet. Res. 5: 171-197.
See also MGI.

Searle, A.G. 1965. Mouse News Letter 32: 39.
See also MGI.

Searle, A.G., and R.I. Spearman. 1957. "Matted," a new hair-mutant in the house mouse: genetics and morphology. J. Embryol. Exp. Morphol. 5: 93-102.
See also MGI.

Shreffler, D.C. 1960. Genetic control of serum transferrin type in mice. Proc. Nat. Acad. Sci. 46: 1378-1384.
See also MGI.

Shreffler, D.C. 1963. Linkage of the mouse transferrin locus. J. Hered. 54: 127-129.
See also MGI.

Shreffler, D.C. 1964a. Inheritance of a serum pre-albumen variant in the mouse. Genetics 49: 629-634.
See also MGI.

Shreffler, D.C. 1964b. A serologically detected variant in mouse serum: further evidence for genetic control by the histocompatibility-2 locus. Genetics 49: 973-978.
See also PubMed.

Shreffler, D.C., and R.D. Owen. 1963. A serologically detected variant in mouse serum: inheritance and association with the histocompatiibility-2 locus. Genetics 48: 9-2.
See also MGI.

Sick, K., and J.T. Nielsen. 1964. Genetics of amylase isozymes in the mouse. Hereditas 51: 291-296.
See also MGI.

Sidman, R.L. 1961. Tissue culture studies of inherited retinal dystrophy. Dis. Nerv. Syst. 22: 1-7.

Sidman, R.L. 1965. Mouse News Letter 32: 37.

Sidman, R.L., M.M. Dickie, and S.H. Appel. 1964. Mutant mice (quaking and jimpy) with deficient myelination in the central nervous system. Science 144: 309-311.
See also MGI.

Sidman, R.L., and M.C. Green. 1965. Retinal degeneration in the mouse. Location of the rd locus in linkage group XVII. J. Hered. 56: 23-29.
See also MGI.

Sidman, R.L., M.C. Green, and S.H. Appel. 1965. Catalog of the Neurological Mutants of the Mouse. Harvard Univ. Press, Cambridge. 82 p.

Sidman, R.L., P.W. Lane, and M.M. Dickie. 1962. Staggerer, a new mutation in the mouse affecting the cerebellum. Science 137: 610-612.
See also MGI.

Silvers, W.K. 1958. Origin and identity of clear cells found in hair bulbs of albino mice. Anat. Rec. 130: 135-144.
See also MGI.

Silvers, W.K., and E.S. Russell. 1955. An experimental approach to action of genes at the agouti locus in the mouse. J. Exp. Zool. 130: 199-220.

Singer, M.F., M. Foster, M.L. Petras, P. Tomlin, and R.W. Sloane. 1964. A new case of blood group inheritance in the house mouse, Mus musculus. Genetics 50: 285-286. (Abstr.)
See also MGI.

Sirlin, J.L. 1956. Vacillans, a neurological mutant in the house mouse linked with brown. J. Genet. 54: 42-48.
See also MGI.

Sirlin, J.L. 1957. Location of vacillans in linkage group VIII of the house mouse. Heredity 11: 259-260.
See also MGI.

Sisken, B.F., and S. Gluecksohn-Waelsch. 1959. A developmental study of the mutation "phocomelia" in the mouse. J. Exp. Zool. 142: 623-642.
See also MGI.

Slee, J. 1962. Developmental morphology of the skin and hair follicles in normal and in ragged mice. J. Embryol. Exp. Morphol. 10: 507-529.
See also MGI.

Slizynski, B.M. 1957. Cytological analysis of translocations in the mouse. J. Genet. 55: 122-130.

Smith, L.J., and K.F. Stein. 1962. Axial elongation in the mouse and its retardation in homozygous looptail mice. J. Embryol. Exp. Morphol. 10: 73-87.
See also MGI.

Smith, P.E., and E.C. MacDowell. 1930. An hereditary anterior-pituitary deficiency in the mouse. Anat. Rec. 46: 249-257.

Snell, G.D. 1928. A cross-over between the genes for short-ear and density in the house mouse. Proc. Nat. Acad. Sci. 14: 926-928.
See also MGI.

Snell, G.D. 1929. "Dwarf," a new mendelian recessive character of the house mouse. Proc. Nat. Acad. Sci. 15: 733-734.
See also MGI.

Snell, G.D. 1931. Inheritance in the house mouse, the linkage relations of short ear, hairless, and naked. Genetics 16: 42-74.
See also MGI.

Snell, G.D. 1945. Linkage of jittery and waltzing in the mouse. J. Hered. 36: 279-280.
See also MGI.

Snell, G.D. 1955. Ducky, a new second chromosome mutation in the mouse. J. Hered. 46: 27-29.
See also MGI.

Snell, G.D. 1958. Histocompatibility genes of the mouse. II. Production and analysis of isogenic resistant lines. J. Nat. Cancer Inst. 21: 843-877.
See also MGI.

Snell, G.D., and H.P. Bunker. 1964. Histocompatibility genes of mice. IV. The position of H-3 in the fifth linkage group. Transplantation 2: 743-751.
See also MGI.

Snell, G.D., M.M. Dickie, P. Smith, and D.E. Kelton. 1954. Linkage of loop-tail, leaden, splotch and fuzzy in the mouse. Heredity 8: 271-273.
See also MGI.

Snell, G.D., and L.W. Law. 1939. A linkage between shaker-2 and wavy-2 in the house mouse. J. Hered. 30: 447.
See also MGI.

Snell, G.D., and L.C. Stevens. 1961. Histocompatibility genes of mice. III. H-1 and H-4, two histocompatibility loci in the first linkage group. Immunology 4: 366-379.
See also MGI.

Sô, M., and Y. Imai. 1926. On the inheritance of ruby eye in mice. Jap. J. Genet. 4: 1-9.
See also MGI.

Spearman, R.I. 1960. The skin abnormality of "ichthyosis," a mutant of the house mouse. J. Embryol. Exp. Morphol. 8: 387-395.
See also MGI.

St. Amand, W., and M.B. Cupp. 1957a. Mouse News Letter 16: 37.
See also MGI.

St. Amand, W., and M.B. Cupp. 1957b. Mouse News Letter 17: 88.
See also MGI.

St. Amand, W., and M.B. Cupp. 1958. Mouse News Letter 19: 38.
See also MGI.

Stein, K.F., and S.A. Huber. 1960. Morphology and behavior of waltzer-type mice. J. Morphol. 106: 197-203.
See also MGI.

Stein, K.F., and J.A. Mackensen. 1957. Abnormal development of the thoracic skeleton in mice homozygous for the gene for looped-tail. Amer. J. Anat. 100: 205-223.
See also MGI.

Stevens, L.C. 1955. Mouse News Letter 13: 41.
See also MGI.

Stevens, L.C. 1963. Mouse News Letter 29: 40.
See also MGI.

Stevens, L.C., and J.A. Mackinsen. 1958. The inheritance and expression of a mutation in the mouse affecting blood formation, the axial skeleton, and body size. J. Hered. 49: 153-160.
See also MGI.

Stevens, L.C., J.A. Mackensen, and S.E. Bernstein. 1959. A mutation causing neonatal jaundice in the hosue mouse. J. Hered. 50: 35-39.
See also MGI.

Stiffel, C., G. Biozzi, D. Mouton, Y. Bouthillier, and C. Decreusefond. 1964. Studies on phagocytosis of bacteria by the reticulo-endothelial system in a strain of mice lacking hemolytic complement. J. Immunol. 93: 246-249.
See also PubMed.

Strong, L.C., and L.B. Hardy. 1956. A new "luxoid" mutant in mice. J. Hered. 47: 277-284.
See also MGI.

Strong, L.C., and W.F. Hollander. 1949. Hereditary loop-tail in the house mouse, accompanied by imperforate vagina and with lethal craniorachischisis when homozygous. J. Hered. 40: 329-334.
See also MGI.

Tansley, K. 1954. An inherited retinal degeneration in the mouse. J. Hered. 45: 123-127.
See also MGI.

Theiler, K. 1957. Boneless tail, ein recessive autosomales Gen der Hausmaus. Arch. Julius Klaus-Stift. Vererb. 32: 474-481.
See also MGI.

Theiler, K. 1959. Anatomy and development of the "truncate" (boneless) mutation in the mouse. Amer. J. Anat. 104: 319-343.
See also MGI.

Theiler, K., and S. Gluecksohn-Waelsch. 1956. The morphological effects and the development of the fused mutation in the mouse. Anat. Rec. 125: 83-104.
See also MGI.

Theiler, K., and L.C. Stevens. 1960. The development of rib fusions, a mutation in the house mouse. Amer. J. Anat. 106: 171-183.
See also MGI.

Thompson, S., J.F. Foster, J.W. Gowen, and O.E. Tauber. 1954. Hereditary differences in serum proteins of normal mice. Proc. Soc. Exp. Biol. Med. 87: 315-317.
See also MGI.

Thomas, G. 1952. Das histologische Verhalten von Milz, Leber, und Knockenmark bei der erblichen Anaemie röntgenmutierter Mäuse. Wiss. A. Martin-Luther-Univ. 1: 13-26.

Tihen, J.A., D.R. Charles, and T.O. Sippel. 1948. Inherited visceral inversion in mice. J. Hered. 39: 29-31.
See also MGI.

Tost, M. 1958. Cataracta hereditaria mit Mikrophthalmus bei der Hausmaus. Z. Mensch. Vererb. Konst. 34: 593-600.
See also PubMed.

Truslove, G.M. 1956. The anatomy and development of the fidget mouse. J. Genet. 54: 64-86.
See also MGI.

Truslove, G.M. 1962. A gene causing ocular retardation in the mouse. J. Embryol. Exp. Morphol. 10: 652-660.
See also MGI.

Tsuzi, S., and T.H. Yosida. 1960. Reciprocal transplantation of skin between rhino and non-rhino mice. Ann. Rep. Nat. Inst. Genet. Jap. (1959) 10: 32.

Tutikawa, K. 1953. Studies on an apparently new mutant, "alopecia periodica" found in the mouse. Ann. Rep. Nat. Inst. Genet. Jap. (1952) 3: 9-10.

Tutikawa, K. 1955. Test for allelism of "alopecia periodica" and "furless" in the house mouse. Ann. Rep. Nat. Inst. Genet. Jap. (1954) 5: 16.

Vankin, L. 1956. The embryonic effects of "blind," a new lethal mutation in mice. Anat. Rec. 125: 648. (Abstr.)
See also MGI.

Verrusio, C. 1964. Mouse News Letter 31: 35.
See also MGI.

Vlahakis, G., and W.E. Heston. 1963. Increase of induced skin tumors in the mouse by the lethal yellow gene (A^y). J. Nat. Cancer Inst. 31: 189-195.
See also PubMed.

Wallace, M.E. 1957a. The use of affinity in chromosome mapping. Biometrics 13: 98-110.

Wallace, M.E. 1957b. A balanced three-point experiment for linkage group V of the house mouse. Heredity 11: 223-258.
See also MGI.

Wallace, M.E. 1958a. New linkage and independence data for ruby and jerker in the mouse. Heredity 12: 453-462.
See also MGI.

Wallace, M.E. 1958b. Experimental evidence for a new genetic phenomenon. Phil. Trans. Roy. Soc. 241: 211-254.

Wallace, M.E. 1959. An experimental test of the hypothesis of affinity. Genetica 29: 243-255.

Wallace, M.E. 1961. Affinity: evidence from crossing inbred lines of mice. Heredity 16: 1-23.

Wallace, M.E. 1963a. Mouse News Letter 28: 22.
See also MGI.

Wallace, M.E. 1963b. Mouse News Letter 29: 22.
See also MGI.

Wallace, M.E. 1965. Mouse News Letter 32: 20.
See also MGI.

Warwick, E.J., and W.L. Lewis. 1954. Increase in frequency of a deleterious recessive gene in mice. J. Hered. 45: 143-145.
See also MGI.

Watney, M.J., and J.R. Miller. 1964. Prevention of a genetically determined congenital eye anomaly in the mouse by the administration of cortisone during pregnancy. Nature 202: 1029-1031.
See also MGI.

Watson, M.L. 1962. A test for the identity of "dysoptic" with "blind" in mice. Proc. Iowa Acad. Sci. 69: 591-593.

Watson, M.L., A. Orr, and T.D. McClure. 1961. A study of blindness in the house mouse. Proc. Iowa Acad. Sci. 68: 558-561.

Webster, L.T. 1937. Inheritance of resistance of mice to enteric bacterial and neurotropic virus infections. J. Exp. Med. 65: 261-286.
See also MGI.

Welshons, W.J., and L.B. Russell. 1959. The Y-chromosome as the bearer of male sex determining factors in the mouse. Proc. Nat. Acad. Sci. 45: 560-566.
See also MGI.

Wolfe, H.G. 1963a. Mouse News Letter 29: 40.
See also MGI.

Wolfe, H.G. 1963b. Two unusual mutations affecting coat color in the mouse, p. 251. In S.J. Geerts [ed.] Proc. XI Int. Congr. Genet. Vol. 1. Pergamon Press, New York. (Abstr.)
See also MGI.

Wolfe, H.G., and D.L. Coleman. 1964. Mi-spotted: a mutation in the mouse. Genet. Res. 5: 432-440.

Wolff, G.L. 1965. Body composition and coat color correlation in different phenotypes of "viable yellow" mice. Science 147: 1145-1147.
See also MGI.

Woolley, G.W. 1941. "Misty," a new coat color dilution in the mouse, Mus musculus. Amer. Natur. 75: 501-508.
See also MGI.

Woolley, G.W. 1945. Misty dilution in the mouse. J. Hered. 36: 269-270.
See also MGI.

Woolley, G.W., and M.M. Dickie. 1945. Pirouetting mice. J. Hered. 36: 281-284.
See also MGI.

Wright, M.E. 1947. Undulated: a new genetic factor in Mus musculus affecting the spine and tail. Heredity 1: 137-141.
See also MGI.

Wunderlich, J., and L.A. Herzenberg. 1963. Genetics of a gamma globulin isoantigen (allotype) in the mouse. Proc. Nat. Acad. Sci. 49: 592-598.
See also PubMed.

Yanagisawa, K., L.C. Dunn, and D. Bennett. 1961. On the mechanism of abnormal transmission ratios at t locus in the house mouse. Genetics 46: 1635-1644.
See also PubMed.

Yoon, C.H. 1959. Waddler, a new mutation and its interaction with quivering. J. Hered. 50: 238-244.
See also MGI.

Yoon, C.H. 1960. Genetic and non-genetic factors affecting the quivering condition in mice. Amer. Natur. 94: 435-440.
See also MGI.

Yoon, C.H. 1961a. Electrophoretic analysis of the serum proteins of neurological mutants in mice. Science 134: 1009-1010.
See also MGI.

Yoon, C.H. 1961b. Linkage relationship of the waddler gene in mice with evidence for temperature effect on crossing-over. J. Hered. 52: 279-281.
See also MGI.

Yoon, C.H., and D.J. Denuccio. 1963. Acid-soluble phosphorus in brains of neurological mice. J. Hered. 54: 202-205.
See also MGI.

Yoon, C.H., and S.R. Harris. 1962. Cholinesterase studies of neurologic mutants in mice. I. Alterations in serum cholinesterase levels. Neurology 12: 423-426.
See also MGI.

Yoon, C.H., and E.P. Les. 1957. Quivering, a new first chromosome mutation in mice. J. Hered. 48: 176-180.
See also MGI.

Yosida, T.H. 1960. Study on the new mutant "falter" found in the house mouse. Ann. Rep. Nat. Inst. Genet. Jap. (1959) 10: 27-28.
See also MGI.

Zimmerman, K. 1933. Eine neue Mutation der Hausmaus: "hydrocephalus." Z. Indukt. Abstamm. Vererb. 64: 176-180.
See also MGI.