Inbred Strains
of Mice: C57BL
Black, a. Origin: Little 1921 from the mating of female 57 with male 52
from Miss Abbie Lathrop's stock. The same cross gave rise to strains C57L
and C57BR. Female 58 mated with the same male gave rise to strain C58.
C57BL is probably the most widely used of all inbred strains, (substrain
C57BL/6 alone accounts for over 14% of occasions on which an inbred strain
is used) though in many ways it seems to be atypical of inbred strains
of laboratory mice. In contrast to 36 other standard inbred strains, it
carries a Y chromosome of Asian
Mus musculus origin (c.f. AKR
and SWR) (
Tucker et al 1992), and a LINE-1
element derived from
Mus spretus the frequency of which suggests
that up to 6.5% of the genome may be of
M. spretus origin (
Rikke et al, 1995). A probe designated B6-38
to the pseudoautosomal region of the X and Y chromosome has a characteristic
Pst I pattern of fragment sizes which is present only in the C57BL family
of strains (
Kalcheva et al, 1995).
It usually has a good breeding performance, depending on substrain, and
has been used as the genetic background for a large number of congenic
strains covering both polymorphic and mutant loci. Four major substrains
A, GrFa, 6 and 10 appear to be quite similar, and any differences are
consistent with what might be expected from the accumulation of new mutations
and a small ammount of residual heterozygosity, though McClive et al (1994) have found that B6 and B10 differ
at multiple loci on chrosome 4 including the microsatellite markers D4Mit69,
D4Mit71 and D4Mit72. Additional microsatellites which distinguish between
B6, B10 and C57BLKS are given by Slingsby et al (1996). The former Ks substrain differs at several loci probably
as a result of genetic contamination with a DBA substrain. This has been
re-named C57BLKS, and is listed separately. The seven major substrains
existing in 1935 are listed below.
C57BL/A
Inbr(A) ?+142. Origin. Little to A c1932. Maint. by A.
C57BL/An
Little to Andervont 1932. Differs from B6 and B10 at the
Ce1 locus.
C57BL/GrFa.
Origin: Little to Gruneberg 1932, to Falconer 1947. Most British substrains
derived from this stock, though 6 and 10 substrains have been imported
more recently. This substrain seems to resemble the 6 rather than the
10 substrain. Maint. by Ola
C57BL/KaLwN.
To N 1965 from Lw at F35. Maint. by N.
C57BL/Ks see C57BLKS
C57BL/6
Inbr (J) 150. Origin: substrains 6 and 10 were separated prior to 1937.
This substrain is now probably the most widely used of all inbred strains.
Substrain 6 and 10 differ at the
H9, Igh2 and
Lv loci.
Maint. by J,N, Ola.
C57BL/10
Inbr (J) 158. Origin: see C57BL/6. Maint. by J.
C57BL/10ScSn.
Inbr (J) ? +136. Little to W.L.Russell to J.P.Scott at F26 as a separate
substrain. To Snell at F35-36. Behaviour differs from C57BL/10J. Maint.
by J,N, Ola.
C57BL/10Cr
Carries spontaneous lipopolysaccharide mutation
lps which appears
to resemble that found in C3H/HeJ (
Vogel et
al 1981).
C57BL/Ola
Carries a spontaneous mutation,
Wlds
, causing a marked slowing of axonal degeneration during Wallerian degeneration
(
Tsao et al, 1994).
Behaviour
Substrain unspecified:
High incidence of tail rattling (1/5) (St. John, 1973).
Short latency to attack and eat crickets (2/7) (Butler,
1973). High alcohol (ethanol) preference ratio (1/5) (McClearn,
1965). Short latency to emerge from home cage (1/7), short latency
to cross barrier in open-field (1/7), low number of stairs climbed (7/7),
low urination (6/7) and defaecation (7/7) (McClearn
et al., 1970., 1970).
C57BL/6
High alcohol (ethanol) preference (1/4) (Fuller, 1964b), (2/18) (
Rodgers,
1966). Achieve blood alcohol levels of 60 mg% when access to alcohol
is restricted to 60 mins. per day (
Le et al, 1994).
Alcohol preference may be associated with strain differences in mesolimbic
enkephalin gene expression (
Ng et al, 1996).
A quasi-congenic QTL introgression strain carrying a low alcohol consumption
gene from BALB/c has lower voluntary alcohol consumption than C57BL/6,
with 96% of loci in common (
Vadasz et al,
1996). Low severity of ethanol withdrawal symptoms compared with DBA/2,
possibly associated with differences in neuroactive steriod sensitivity
(
Finn et al, 1997). Alcohol preference is
due to at least two recessive quantitative trait loci that are sex-restricted
in expression (
Melo et al, 1996).
Low `emotionality' (12/15), high open-field exploration (2/15) (Thompson,
1953). High spontaneous locomotor activity (8/9) (Nikulina et al 1991). Short time of immobility in a forced
swimming test (8/9) (Nikulina et al 1991).
Low shock-avoidance learning (7/9) (Bovet et
al., 1966., 1966, 1969). Low shuttle-box avoidance (5/5), high wheel
activity (1/5) (Messeri et al., 1972.,
1972). Rapid shock-avoidance learning (2/7) and slow extinction (6/7)
(Schlesinger and Wimer, 1967). High
shock-avoidance learning (1/8) (Wahlsten, 1973).
High radial-arm maze learning (1/3) (Ammassari-Teule
et al, 1993).
High locomotor activity (1/5) (Davis and King,
1967). High locomotor activity when grouped (2/6) and single (1/6)
(Davis et al., 1967., 1967). Resistant
to audiogenic seizures (11/11) (Fuller and
Sjursen, 1967). Relatively insensitive to the primary odorant isovaleric
acid (contrast seven other strains) and may provide an animal model of
specific anosmia (Wysocki et al., 1977.,
1977). Low balsa-wood gnawing activity (2/16) Fawdington and Festing (1980).
High preference for sweet tasting substances (saccharin, sucrose, dulcin
and acesulfame, averaged) (1/26) (Lush 1988).
Rejects saline at moderate concentrations (contrast 129) (Beauchamp and Fisher, 1993,
Gannon and Contreras, 1995). Feed restriction for nine days failed
to cause stereotypic cage cover climbing (contrast DBA/2) (Cabib and Bonaventira, 1997).
C57BL/10
High open-field activity (3/15) (
Thompson, 1953).
High alcohol preference (6/18) (
Rodgers, 1966).
Good water escape learning (1/6) (Festing 1973b). Good performance in
food-seeking task (1/6) (
Henderson, 1970).
Insensitive to the odour of isovaleric acid (see C57BL/6). High preference
for sweet tasting substances (saccharin, sucrose, dulcin and acesulfame,
averaged) (4/26) (
Lush 1988).
Life-span and spontaneous disease
Substrain unspecified:
Mammary tumours less than 1% (Heston and Vlahakis,
1971). Lung adenomas 0-9% in LiA substrain (Mühlbock and Tengbergen,
1971). Zero incidence of mammary tumours at 2 years (cf. 3/7) (Bentvelzen et al., 1970., 1970).
Mean life-span 800 days in males and 750 days in females according to Rowlatt
et al. (1976), who also give
details of pathology in a large aging colony of C57BL/Icrf-at
mice. Hyperphalangy and polydactyly occur with a low incidence in all
C57BL strains and substrains (Dagg, 1966). Hydrocephalus
4.1% (Mori, 1968). Type B reticulum cell neoplasms
75% at about 20 weeks in HeDe substrain (Dunn
and Deringer, 1968).
C57BL/Ka
Median life-span 23 months in males. Main autopsy findings include reticulum
cell sarcoma type B (29%), testes interstitial tumour (13%), thyroid follicular
adenoma (9%), unclassified lymphoreticular tumours (9%). Nine other tumour
types found. Non-neoplastic lesions include amyloid (83%), Sendai virus
pneumonia (20%), periarteritis nodosa (16%), mesenteric disease (10%).
Several other lesions noted. (Zurcher
et al., 1975). About 50%
of mice develop homogeneous immunoglobulins resembling idiopathic paraproteinaemia
in man by 24 months (Radl and Hollander, 1974).
C57BL/Fa
Long life-span in males (14/17 = 645 days), but intermediate in females
(5/17 = 580 days) in SPF fostered conditions (
Festing
and Blackmore, 1971). Hydronephrosis 0.5% in females, 1.5% in males
(
Taylor and Fraser, 1973).
C57BL/6
Primary lung tumours 1% in males, 3% in breeding females and zero in virgin
females. Lymphatic leukaemia less than 2%, mammary adenocarcinomas less
than 1% (
Hoag, 1963). Leukaemia 7% (
Myers et al., 1970., 1970). Rare "lipomatous" hamartomas
or choristomas have been noted (
Adkison et
al 1991).
Susceptible to the development of atheromatous lesions on wall of aorta
after 20 weeks on a high-fat diet (Thompson, 1968; Roberts and Thompson, 1976). Develop fatty
streak-like lesions in the valve sinus region of the ascending aorta after
10-20 weeks on a diet enriched in saturated fat and cholesterol. After
a further 15 weeks fibro-fatty lesions with many of the characteristics
of human atheromatous plaques are found (Stewart-Phillips and Lough 1991). Exhibit aortic cartilaginous
metaplasia (contrast C3H) (Qiao et al, 1995).
Susceptible to diet-induced aortic fatty streak lesions which correlates
with a low level of paroxinase mRNA (contrast C3H) (Shih et al, 1996).
Develops non-insulin-dependent diabetes mellitus and hypertension when
fed a high fat-high simple carbohydrate diet, whereas A/J mice do not
(Mills et al 1993). Susceptible to the
development of atherosclerosis on a semi-synthetic high fat diet (1/9)
(Nishina et al, 1993). Blood glucose
levels and insulin insensitivity in crosses between diet-induced type
II diabetes sensitive C57BL/6 and resistant A/J are genetically independent
(Surwit et al 1991). High simple carbohydrate
diet for five months induced hyperglycemia, hyperinsulinemia and hypercholesterolemia
and non-insulin-dependent diabetes mellitus which appeared to be associated
with the metabolic characteristics of visceral fat (Rebuffe-Scrive et al, 1993). Gain more weight on high fat
diets without consuming more calories than A/J mice and develop adipocyte
hyperplasia. However, animals fed a low fat, high sucrose diet were leaner
than those fed a high-complex-carbohydrate diet. These results suggest
that genetic differences in metabolic response to fat is more important
in the development of obesity and diabetes than caloric intake (Surwit et al, 1995). Loci on chromosomes 1, 3, 5 and 11
are associated with variation in high density lipoprotein levels with
coordinate expression of cholesterol-7-alpha hydroxylase in a cross involving
atherosclerosis resistant C3H/HeJ mice (Machleder
et al, 1997). Hepatic stearoyl CoA desaturase mRNA levels significantly
elevated compared with atherosclerosis-resistant BALB/c mice, and was
reduced in mice fed a high fat diet (Park et
al, 1997).
Congenital abnormalities 10%, including eye defects, polydactyly and otocephaly
(Kalter, 1968). Microphthalmia and anophthalmia
8-20% and hydrocephalus 1-3% (Dagg, 1966). Occular
defects appear to be due to defects in development of the lens (Robinson et al, 1993).
Develop spontaneous auditory degeneration with onset during young adulthood,
with enhanced susceptibility to acoustic injury and delayed effects of
toluene (contrast CBA/Ca) (Li, 1992, Willott et al, 1993, Li et al,
1993, Li and Borg, 1993). This is associated
with early hair cell changes including bent and fused stereocillia, bulging
of the cuticle plates, hair cell loss and swelling of affected dendrites
(Hultcrantz and Li, 1993). Carry a
single recessive gene different from that found in BALB/cBy and WB/ReJ,
causing age-related hearing loss (Willott
et al, 1995). Hearing loss is caused by degeneration of the organ
of Corti, originating in the basal, high frequency region and then proceeding
apically over time. This results in a severe sensorineural hearing loss
by 14 months of age (Walton et al, 1995).
More susceptible to noise-induced hearing loss than CBA/J (Erway et al, 1996).
Life-span above average in both sexes in conventional conditions (17/22
= 676 days in males, 18/22 = 692 days in females) (Storer,
1966). Life-span 827 _ 34 days in males, 818 _ 21 days in females
(Goodrick, 1975). Life-span 878 _ 10 days
in males and 794 _ 6 days in females (Kunstyr
and Leuenberger, 1975). Median life-span 600 days (Curtis,
1971). Gross tumour incidence 70%, maximum life-span about 1200 days
in SPF conditions (Mewissen, 1971).
Dermatitis with intense pruritis leading to self-mutilation and death,
and sometimes associated with the mite Myobia musculi appears
to be more severe in this strain than others (Csiza
and McMartin, 1976). Impaired axonal regeneration involving multiple
genetic loci (Lu et al, 1994)
C57BL/10
Long life-span (826_29 days in males, 693_31 days in females). Overall
tumour incidence 33% in males and 31% in females, most of which is due
to lymphoma (31% in males, 29% in females) (
Smith
et al., 1973., 1973). Microphthalmia and anophthalmia 8-20% and hydrocephalus
1-3% (
Dagg, 1966). Dermatitis leading to self-mutilation
as described in C57BL/6 is also common in this substrain. Incidence may
reach 4% (Sparrow, personal communication).
Normal physiology and biochemistry
Substrain other than /6 or /10
High thyroid activity (1/5) (Van Heyningen, 1961).
Mammary gland insensitive to oestradiol and progesterone (6/7) (Singh et al., 1970., 1970). Low brain aromatic L- amino
acid decarboxylase (5/5) and low acetylcholinesterase activity (5/5) (Pryor et al., 1966., 1966). Blood catalase
has a low specific activity (6/7) (Magdon, 1962).
Low hind foot pad (9/9) but high (1/9) tail temperature (Shepard and Habas, 1967). High serum calcium (2/6) (Barrett et al., 1975., 1975). Low erythrocyte
catalase (12/18 to 17/18, depending on substrain) (Hoffman and Rechcigl, 1971). High basal level of serum prolactin
(1/6) (Sinha et al., 1975., 1975). Resistant
to dietary induction of obesity (Fenton and
Dowling, 1953). High level of alpha-fetoprotein in plasma at 7 days
(1/6) (Adinolfi et al 1990).
C57BL/6
Low plasma cholesterol at 12 and 24 weeks (8/8) (
Weibust,
1973). Low plasma triglyceride levels (1/11 in By and 3/11 in J substrains)
and low plasma cholesterol (2/11 in By and 4/11 in J substrains) (
Jiao et al 1990). Low serum ceruloplasmin levels in males
(24/26) but intermediate in females (
Meier
and MacPike, 1968). High blood sugar (3/12) (
Nishimura,
1969). Low serum cholesterol (5/5) in C57BL/6-
ata
(
Bruell et al., 1962., 1962). Arterial
blood has a low pH (10/10) (
Bernstein, 1966).
Low concentration of prostaglandin F in epididymis (6/6) (
Badr,
1975). High liver tyrosine aminotransferase in fasted mice (3/10)
but low in C57BL/6-
ob (10/10) (
Blake, 1970).
Low brain
L-glutamic acid decarboxylase (GAD) (7/7) and acetylcholinesterase
activity (7/7) but high catechol-
O-methyltransferase activity
(2/7) (
Tunnicliff et al., 1973., 1973).
Low calcium uptake by the heart (4/5) (
Mokler
and Iturrian, 1973). Low sensitivity to thyrotropin (20/21) (
Levy et al., 1965., 1965). High brain sulphatide (1/5)
(
Sampugna et al., 1975., 1975). High
hepatic benz (alpha) pyrene hydroxylase activity (1/6) (
Kodama and Bock, 1970). Low hepatic delta-aminolaevulinate
dehydratase activity (8/8) (
Doyle and Schimke,
1969). High aldehyde dehydrogenase and alcohol dehydrogenase activity
compared with DBA/2 (
Sheppard et al., 1968.,
1968). High metabolism of
131I with low 48 h retention (1/6)
(
Chai et al., 1957., 1957). High liver arylsulphatase
activity (1/12) (
Daniel, 1976). Low porphyrin
content of Harderian gland (16/16) (
Margolis,
1971). Low hepatic urokinase activity (4/6 to 6/6) but high hepatic
histidine ammonia-lyase activity (1/6 to 2/6 in two substrains) (
Hanford et al., 1974., 1974). Low basal levels of kidney
catalase (4/4), superoxide dismutase (4/4) and renal glutathione reductase
(4/4) (
Misra et al 1991). Iron overload
causes inhibition of hepatic uroporphyrinogen decarboxylase and uroporphyria
in C57BL/10ScSn but not DBA/2 mice. This was not correlated with the Ah
locus in a study involving 12 mouse strains (
Smith
and Francis, 1993). Low levels of apoA-IV messenger RNA in liver compared
with 129/J (
Reue et al, 1993)
Low susceptibility to audiogenic seizures (6/6) (Deckard
et al., 1976., 1976). Long tau DD, the endogenous (free-running) period
of the circadian pacemaker measured in constant environmental darkness
(12/12) (Schwartz and Zimmerman 1990)
Has defective secretory group II phospholipase A2 gene (cf strains 129/Sv
and B10.RIII) (Kennedy et al, 1995).
Susceptible to severe hypercapnia with hypoxia assessed by elevated minute
ventilation rate (1/8) (Tankersley et
al, 1994). Has a rapid and shallow breathing pattern phenotype (contrast
C3H) (Tankersley et al, 1997). Susceptible
(1/7) to cerebral ischemia following bilateral carotid occlusion with
90% of mice showing typical neuological signs such as torsion of the neck
and rolling fits with selective neuronal death in the hippocampus and
caudoputamen after 20 minutes of ischemia (Yang
et al, 1997).
C57BL/10
Low plasma testosterone level (4/5) (
Hampl et
al., 1971., 1971). High Na/K ratio in erythrocytes (3/9) and plasma
(2/9) (
Waymouth, 1973). Low serum ceruloplasmin
levels in males (25/26) but intermediate in females (
Meier and MacPike, 1968). Low systolic blood pressure (18/19)
(
Schlager and Weibust, 1967). Low brain
glutamic acid decarboxylase in B10.BR (10/10) and ScSn substrains (9/10)
(
Gaitonde and Festing, 1976). Resistant
to electroconvulsive seizures (6/6) (
Deckard
et al., 1976., 1976). Iron overload causes inhibition of hepatic uroporphyrinogen
decarboxylase and uroporphyria in C57BL/10ScSn but not DBA/2 mice. This
was not correlated with the
Ah locus in a study involving 12
mouse strains (
Smith and Francis, 1993).
Anatomy
Substrain unspecified
Low proportion of basophilic cells in adenohypophysis (5/5) (Keramidas and Symeonidis, 1973).
C57BL/6
Small kidney/body weight ratio (19/21) (
Schlager,
1968). Large thyroid (1/5) (
Mendoza et
al., 1967., 1967). High total leukocyte count (2/18), low erythrocyte
count (14/18) (
Russell et al., 1951.,
1951). Small hippocampus (9/9) (
Wimer et al.,
1969., 1969). Accessory spleens in about 32% of mice (2/9) and low
number of Peyer's patches (7/7) (
Hummel et
al., 1966., 1966). Higher bone mass than A/J (
Kaye
and Kusy, 1995). Low number of haematopoetic stem cells in bone marrow
(contrast DBA/2) (Muller-Sieburg and Riblet, 1996).
Less susceptible to the development of micronuclei than BALB/c following
treatment with clastogenic base analogues and nucleosides (Sato et al, 1993). High level of spontaneous sister chromatid
exchange (4/4) (Nishi et al, 1993). A detailed
staging of these mice between gestation days 11 and 13 (Theiler's stages
18 and 21) has been published by Miyake et al, (1996). Hematopoetic stem-cell
pool 11-fold lower than in DBA/2. This is largely due to loci on chromosome
1 (Mullersieburg and Riblet, 1996). Low bone density of femur (11/11)
(Beamer et al, 1996). The timing of onset
and duration of condensation and onset of matrix formation of first arch
cartilages has been described by Miyake et al (1996a).
A detailed staging table to facilitate study of cranial skeletal development
every 2hrs. between days 11 and 13 of gestation has also been described
(Miyake et al, 1996b)
C57BL/10
Small kidney/body weight ratio (21/21) (
Schlager,
1968). High number of bristles on foot pad (1/8 to 3/8 in three congenic
lines) (Festing, 1976a). High yield of peritoneal exudate cells (1/5)
with a high percentage of macrophages (1/5), low percentage of lymphocytes
(5/5) and high granulocytes (1/5) (
Schwartz
et al., 1975., 1975).
Drugs
Substrain unspecified
Resistant to induction of adenocarcinomas of the colon by 1, 2-dimethylhydrazine
(cf. 2/4) (Evans et al., 1974., 1974).
Resistant to induction of pulmonary tumours (6/6) and leukaemia (5/6)
by neonatal administration of DMBA (Flaks, 1968).
Susceptible to the induction of pulmonary fibrosis by bleomycin (contrast
C3Hf/Kam) (Haston et al, 1996) and irradiation,
though the sensitivity of lung fibroblasts to irradiation in-vitro
does not correlate with in-vivo sensitivity (Dileto and Travis, 1996).
Sensitive to the development of uterine tumours following treatment with
DMBA at 4-weeks of age (cf 3/6) (Tsubura
et al, 1993). Resistant to induction of mammary tumours by urethane
(7/7) (Bentvelzen et al., 1970., 1970).
Pituitary adenoma induced in most mice by oestrogens (Heston,
1963). Resistant to skin tumour induction by methylcholanthrene (5/5)
(Andervont and Edgcomb, 1956). Susceptible
to fibrosarcoma induction by methylcholanthrene (4/15 males, 3/15 females)
(Strong, 1952).
Resistant to chloroform toxicity (cf. 5/9) (Deringer
et al., 1953., 1953). Resistant to induction of cleft palate by cortisone
(4/5) (Kalter, 1965).
Resistant to lethal effects of ozone (22/22) (Goldstein
et al., 1973., 1973). Resistant to colon carcinogenesis by 1,2-dimethylhydrazine
(cf. 4/7) (Evans et al., 1977., 1977).
C57BL/Fa
Resistant to induction of lung tumours by urethane (6/6) (
Falconer and Bloom, 1962). Insensitive to insulin (8/9),
sensitive to histamine (2/9) (
Brown, 1965).
C57BL/6
Susceptible to skin ulceration by DMBA (cf. 13/22) (
Thomas et al., 1973., 1973). Susceptible to induction of subcutaneous
tumours by 3-methylcholanthrene (3/14) (
Kouri
et al., 1973., 1973), (1/12) (
Whitmire
et al., 1971., 1971). High incidence of lymphomas after methylcholanthrene
administration by gavage (2/5) (Akamatsu and Barton, 1974). Susceptible
to toxic effects of DMBA (6/6) (
Schmid et
al., 1966., 1966). Pre-treatment with beta-naphthoflavone 48 hr. before
administration of N-nitrosoethylurea (ENU), once weekly for 4 weeks caused
a significant doubling in the number of lung tumor bearers (contrast 4
strains) (
Anderson et al 1990). Phenobarbitone
in the diet to give an intake of 85mg/kg per day resulted in 4% of animals
developing basophilic nodules by 91 weeks of age (contrast 70% in C3H/He),
but no increase in liver carcinomas (
Evans
et al, 1992). However, there was a two-fold lower level of DNA synthesis
in C57BL/6 mice relative to C3H mice after partial hepatactomy, though
partial hepatectomy is a tumour promoter in C57BL/6 but not in C3H mice
(
Bennett et al, 1995).
Sensitive to teratogenic effects of acetazolamide (2/6) (Green et al., 1973., 1973). Resistant to teratogenic effect
(cleft palate) by cortisone acetate (2/6) (Kalter 1981). Hepatic epoxide
hydrase activity induced by pentobarbital i.p. (cf. 4/7) (Oesch et al., 1973., 1973). Resistant to teratogenic effects
of cortisone acetate (4/4) (Dostal and Jelinek,
1973). Resistant to lethal effects of ozone (16/21) (Goldstein et al., 1973., 1973), but susceptible (cf 5/8)
to ozone-induced decreases of tracheal potential (Takahashi et al, 1995) and to airway inflammation (contrast
C3H/He) (Kleeberger et al, 1993).
Susceptible to ozone-induced lung inflammation, which is exacerbated by
vitamin A deficiency (Paquette et al, 1996).
High incidence of convulsions induced by flurothyl (1/5) (Davis and King, 1967). Susceptible to hyperbaric oxygen
(4/18) (Hill et al., 1968., 1968). Resistant
to chloroform toxicity (cf. 5/9) (Hill et al.,
1975; Deringer et al., 1953 al.,
1953). Resistant to toxic effects of isoniazid (2/10) (Taylor 1976b).
Sensitive, as judged by eosinophil response, to cortisone acetate (cf.
3/6) (Wragg and Speirs, 1952). High (89%)
ovulatory response to 3 I.U. of PMS in immature mice (2/6), but only a
56% response to 7 I.U. No facilitation by exposure to males at these doses
(Zarrow et al., 1971., 1971). High locomotor
activity after treatment with D-amphetamine (1/6) (Babbini et al., 1974., 1974). Nicotine increases learning
ability (1/9) (Bovet et al., 1966., 1966).
Resistant to colon carcinogenesis by 1,2-dimethylhydrazine (cf. 4/7) (Evans et al., 1977., 1977). Low ED50 to behavioural
effects of nicotine (3/19) (Marks et al 1989).
High self-selection of nicotine (1/6) which is inversely correlated with
sensitivity to nicotine-induced seizures (Robinson
et al, 1996).
Low bronchial reactivity (6/6) to methacholine and serotonin (Konno et al 1993). Resistant (6/8) to daunomycin-induced
nephorsis (Kimura et al 1993). Low (10/10)
neural sensitivity to pentylenetetrazol convulsions (Kosobud et al 1992). Susceptible to biliary tract injury
following oral dosing with 500 micrograms of the fungal toxin sporidesmin
(1/4) (Bhathal et al 1990). Low histamine
release from peritoneal mast cells induced by compound 48/80, a calcium
dependent histamine releaser ( c.f. 5/8) (Toda
et al 1989). Low histamine release from peritoneal mast cells induced
by Ca2+ ionophore A23187 ( c.f. 1/8, contrast BALB/c, C3H/He, DBA/2 etc.)
(Toda et al 1989). Carries gene (Tpmt)
for low levels of thiopurine methyltransferase activity, catalyzing the
S-methylation of 6-mercaptopurine and other heterocyclic and
aromaticthiol compounds (like AKR, unlike DBA/2) (Otterness and Weinshilboum 1987a,b). More sensitive to
acute toxic effects of aflatoxin B-1 than strains CBA/J or BALB/c (Almeida et al, 1996).
Airways hyporeactive to acetylcholine (c.f. 3/7) (Zhang
et al, 1995). High voluntary comsumption of morphine in two-bottle
choice situation (1/15) (Belknap et al, 1993).
Estrogen induces an increase in VLDL and LDL-cholesterol (like C57L,
contrast BALB/c and C3H) (Srivastava, 1995).
Nine-fold higher ED50 for haloperidol-induced catalepsy than DBA/2, but
this is not associated with numbers of cholinergic neurons (Dains et al, 1996). Accumulates three to five-fold lower
levels of mercury in liver and blood than DBA/2 or A.SW after 4 weeks
exposure to mercuric chloride, but higher levels in spleen following 8-12
weeks of exposure (Griem et al, 1997).
C57BL/10
Nicotine decreases shock-avoidance learning (8/9) (
Bovet
et al., 1966., 1966). Low ED50 to behavioural effects of nicotine
(1/19) (
Marks et al 1989). Congenic line
B10.BR susceptible to induction of subcutaneous tumours by 3-methylcholanthrene
(
Kouri et al., 1973., 1973).
Immunology
Substrain unspecified
Poor immune response to low levels of bovine gamma-globulin (cf. 4/8) (Levine and Vaz, 1970). Poor primary immune
response to bovine serum albumin (6/6) (James
and Milne, 1972). Poor primary immune response to sheep erythrocytes
(3/6 to 6/6, depending on test and dose) (Ghaffar
and James, 1973). Poor immune response to Vi antigen (cf. 3/5) (Gaines et al., 1965., 1965). Low antibody
affinity (7/7) and small quantity of antibody production (6/7) (Alpers et al., 1972., 1972). Low antibody affinity to HSA
(9/9) (Petty et al., 1972., 1972).
C57BL/Fa
Serum anti-nuclear factor in 12% of animals tested (5/17) (
Barnes and Tuffrey, 1967). Good primary immune response
to bacteriophage fd (2/7) (Kolsch
et al., 1971).
C57BL/6
High susceptibility to induction of amyloid by casein (1/6) (
Willerson et al., 1969., 1969). Poor immune response to
type III pneumococcal polysaccharide (4/5) (
Braley
and Freeman, 1971). Poor immune response to synthetic double- stranded
RNA (6/7) (
Steinberg et al., 1971.,
1971). Good immune response to cholera A and B antigens (2/8) (
Cerny et al., 1971., 1971). Resistant to induction of anaphylactic
shock by ovalbumin (cf. 6/13) (
Tanioka and
Esaki, 1971). Rapid rejection of about 76% of male skin isografts
by females by 25 days (1/10) (
Gasser and Silvers,
1971). Poor immune response to GAT (random terpolymer of Glu
60,
Ala
30, Tyr
10) (9/10) (
Dorf
et al., 1974., 1974). Good immune response to
Salmonella senftenberg
(1/5) and
S. anatum (2/5) lipopolysaccharide (
Di
Pauli, 1972). Non-responder to synthetic polypeptide Glu
57,
Lys
38, Ala
5 (cf. 4/7) (
Pinchuck
and Maurer, 1965). High sporadic occurrence of natural haemagglutinins
to sheep red blood cells (
Brooke, 1965). Discriminator
between `H' and `L' sheep erythrocytes (cf. 12/18) (
McCarthy and Dutton, 1975). Poor immune response to Pro-Gly-Pro-ovalbumin
(7/7) and (Pro
66, Gly
34)
n (6/7) but good
immune response to (Pro-Gly-Pro)
n (1/17) (
Fuchs et al., 1974., 1974). High (2/6) PHA- stimulated lymphocyte
blastogenic response (
Hellman and Fowler,
1972). Erythrocytes have low agglutinability (cf. 11/25) (
Rubinstein et al., 1974., 1974). High immune response to
ferritin in B6-
Tla (2/16) (
Young et
al., 1976., 1976). Low responder to dextran (cf. 6/10) (
Blomberg et al., 1972., 1972). Low responder to
E.
coli ß-D-galactosidase, with "memory" developing in absence
of antibody formation (
de Macario and Macario
1980). Precipitating and skin sensitising antibodies have slow electrophoretic
mobility (6/6) (
Fahey, 1965). Resistant to anaphylactic
shock (
Treadwell, 1969). Susceptible (1/5)
to induction of autoimmune prostatisis (contrast BALB/c) (
Keetch et al, 1994). High expression of neutral glycosphingolipid
GgOse(4)Cer in concanavalin A stimulated T lymphoblasts (cf 3/6) (
Muthing,
1997).
Anti-BPO IgE monoclonal antibody produced potent systemic sensitization
sufficient for provocation of lethal shock in most aged (6 to 10 months)
mice (c.f. 3/8) (Harada et al 1991). Susceptible
to immunosuppression of contact hypersensitivity by ultraviolet B light
(cf 3/18) (Noonan and Hoffman, 1994).
C57BL/10
High lymphocyte phytohaemagglutinin response (10/43) (
Heiniger et al., 1975., 1975). Rejection of 70% of male
skin isografts by females by 25 days (2/10) (
Gasser
and Silvers, 1971). Poor immune response to ovomucoid, but good immune
response to ovalbumin (cf. 6/12) (
Vaz et al.,
1971., 1971). Poor immune response to DNP-keyhole limpet haemocyanin
(10/11) (
Borel and Kilham, 1974). Non-responder
to synthetic polypeptide Glu
57, Lys
58, Ala
5
(cf. 4/7) (
Pinchuck and Maurer, 1965).
Low antibody affinity (6/7) and small quantity of antibody produced (7/7)
in B10.D2-
n (
Alpers et al., 1972.,
1972). Discriminator between `H' and `L' sheep erythrocytes (cf. 12/18).
Also in B10.BR and B10.D2-
n (
McCarthy
and Dutton, 1975). Low IgM antibody response to sheep red blood cells
compared with A/J (
Vetvicka et al, 1993).
Resistant to induction of passive cutaneous anaphylaxis (IgG
1-
and IgE- mediated) (12/12) (
De Souza et al., 1974.,
1974). Erythrocytes have low agglutinability (cf. 11/25) (
Rubinstein et al., 1974., 1974). High immune response to
ferritin in B10 (4/16) and congenic lines B10.M (1/16), B10.D2 (3/I6),
B10.BR (5/16) and B10.A (6/16) (
Young et al.,
1976., 1976). Susceptible to immunosuppression of contact hypersensitivity
by ultraviolet B light (cf 3/18) (
Noonan and
Hoffman, 1994). High neutrophil response to thioglycolate broth and
killed bacteria (contrast BALB/c) (
Marley
et al, 1994). Moderate susceptibility to experimental allergic encephalomyelitis
with long (1/10) duration (
Lindsey, 1996).
Infection
Substrain unspecified
Resistant to oncogenic effects of polyoma virus given at birth (Law,
1966a). Resistant to Mycobacterium marinum (2/9) and poor
plateau harvest of M. leprae 8 months after infection (9/9) (Shepard and Habas, 1967).
C57BL/Fa
Highly susceptible to infection by
Salmonella typhimurium strain
C5 (2/7) (
Plant and Glynn, 1974).
C57BL/6
Develops a slowly progressing parasitosis ("low responder") after infection
with the Cornell strain of
Toxoplasma gondii (
Macario et al 1980). Did not support sustained growth of
six strains of
Leishmania mexicana mexicana (contrast BALB/c)
(
Monroy-Ostria et al, 1994). Resistant
to
Leishmania major (contrast BALB/c) (
Laskay
et al, 1995, Scott et al, 1996). Susceptible
to
L. major mexicana, and vaccination against the parasite using
liposomes with parasite membrane antigens was effective (cf CBA/Ca but
contrast C57BL/10) (Lazama-Davila, 1997).
Susceptible to Salmonella typhimurium strain C5 (1/5) (Robson and Vas, 1972). 100-fold more resistant to Listeria
monocytogenes than A/J when measured by median lethal dose (Sadarangani et al 1980). This seems to be associated with
increased levels of gamma interferon and granulocyte-macrophage colony
stimulating factor compared with susceptible A/J mice (Iizawa et al, 1993). Resistant to Mycoplasma fermentens
(6/6) (Gabridge et al., 1972.,
1972). Resistant to Mycoplasma pulmonis infection (cf 4/16) (Cartner et al, 1996).Resistant to infection
by Mycobacterium marinum (6/6) (Yamamoto
et al 1991). Resistant to infection by liver fluke Opisthorchis
felineus (6/6) (Zelentsov, 1974). Resistant
(1/4) to infection with the helminth worm Angiostrongylus costaricennsis
(Ishii and Sano 1989). Relatively susceptible
to infection with Helicobacter felis (contrast C57BL/6) (Mohammadi et al, 1996). Susceptibile to infection by Helicobacter
felis with moderate to severe chronic active gastritis in the body
of the stomach, which increased over time (cf 4/6) (Sakagami et al, 1996). H. felis induces hypertropic
gastropathy (Fox et al, 1996).
Highly resistant to the mammary tumour virus which is thought not to be
carried by the strain (Murray and Little,
1967). Resistant to Herpes simplex virus (2/11) (Lopez,
1975). Resistant to herpes simplex virus-1 (contrast BALB/c) (Brenner et al, 1994).. Susceptible to mouse hepatitis virus
type 3 infection (cf. 5/14) (Le Prevost et al.,
1975., 1975). Develops antibodies to mouse hepatitis virus which can
be reliably detected by the complement fixation test, in contrast to five
other strains (Kagiyama et al 1991).
Low mortality in a natural epizootic of ectromelia (7/8) (Briody,
1966). High expression of RNA tumour virus group-specific antigen
in some substrains (1/8) but low in others (7/8) (Whitmire and Salerno, 1972). Resistant to development of leukaemia
on infection by Friend virus (cf. 2/11) (Dietz
and Rich, 1972). Resistant to diabetogenic effects of encephalomyocarditis
virus, but treatment with carrageenan to compromise macrophage function
makes the mice susceptible (Hirasawa et
al, 1995). Susceptible to measles virus induced encephalitis, which
correlates with a high cytotoxic T-lymphocyte response (like C3H, contrast
BALB/c) (Niewiesk et al, 1993). Resistant
to the development of tumours following inoculation with polyoma virus
(Freund et al, 1992).
Resistant (6/7) to the development of chronic Chagas' cardiomyopathy in
postacute Trypanosoma cruzi infection (Rowland
et al 1992). Resistant to infection with Trypanosoma congolense
with an initial peak of parasitemia on day 6, followed by rapid apparent
clearance in an average of 3 days (contrast BLAB/c) (Ogunremi and Tabel, 1995). Infection with larval Echinococcus
multilocularis by transportal injection of hyatid homogenate results
in a multivesiculation form of hyatid development (cf 4/9) (Nakaya et al, 1997).
Resistant to tumorigenesis induced by polymoa virus (1/9), in contrast
with C3H/Bi (Freund et al 1992). Susceptible to mouse adenovirus type
1 which causes a fatal hemorrhagic encephalomyelitis (contrast BALB/c)
(Guida et al, 1995).
Less susceptible to Streptococcus suis type 2 including the type
strain, two isolates from meningitis in pigs and two isolates from tonsils
of clinically healthy pigs (c.f. 3/5) (Kataoka
et al 1991). Resistant to carditis on infection with Lyme borreliosis
(Borrelia burgdorferi) (contrast C3H, SWR, BALB/c) (Barthold et al 1990). Thymectomized C57BL/6 mice that were
intravenously infused with monoclonal antibody to selectively deplete
CD4+ T cells are susceptible to disseminated Mycobacterium avium
infection. The increased susceptibility is comparable to that of C57BL/6-bg.
The course of such infections can be markedly restrained and in some
cases the infections can be sterilized by treatment over a 120-day period
with the antimycobacterial agent rifabutin (Furney
et al 1990). Susceptible to infection with M. avium strains
101 and 2-151, and can be used to test anti-mycobacterial agents (Furney et al, 1995). Susceptible to infection with M.
paratuberculosis (contrast C3H/HeJ) (Tanaka
et al, 1994). Resistant to infection with Yersinia enterocolitica
associate with a good interferon gamma response (contrast BALB/c) (Autenrieth et al, 1994).
Susceptible, with high amylase response to the fungus Paracoccidioides
brasiliensis (cf 6/12) (Xidieh et al,
1994)
Mouse mammary tumor proviral loci have been identified by Lee and Eicher
(1990). Resistant (1/10) to infection with
Ehrlichia risticii (Williams and
Timoney, 1994). Highly susceptible to Plasmodium berghei
with all mice developing erythrocytic infection following intravenous
injection of 50 sporozoites. The same level of infection could only be
established in BALB/c with 10,000 sporozoites (Scheller
et al, 1994). Infection with P. berghei results in low blood
parasitemia and death with neuological symptoms within 8-10 days, in contrast
with the more resistant BALB/c (Moumaris
et al (1995). Resistant to chronic weakness and inflammation following
infection with Tucon strain of coxsackie virus B1, in contrast with C57BL/10
and B10 congenic strains (Tam and Messner, 1996).
C57BL/10
Congenic line B10.D2-n is highly susceptible to infection by
Salmonella
typhimurium strain C5 (3/7) (
Plant and
Glynn, 1974). Resistant to
Herpes simplex virus (2/Il) (
Lopez, 1975). B10.D2-
o is susceptible to
mouse hepatitis virus type 3 infection (cf. 5/14) (
Le
Prevost et al., 1975., 1975). Slow immunological expulsion of
Trichinella
spiralis worms (
Wakelin and Donachie
1980). Following administration of murine cytomegalovirus, C57BL/10
and B10.BR mice developed myocarditis after neonatal infection, but inflammation
resolved rapidly after adult infection and age-related cardiopathy was
correspondingly mild. (contrast BALB/c, C3H) (
Price
et al 1991). Resistant to infection with the helminth
Mesocestoides
corti (contrast SJL, NIH) (
Lammas et
al 1990). Resistant (2/10) to infection with
Ehrlichia risticii
(
Williams and Timoney, 1994). Susceptible
to chronic weakness and inflammation following infection with Tucon strain
of coxsackie virus B1, in contrast with C57BL/6 (
Tam
and Messner, 1996). Resistant to
Mycoplasma pulmonis infection
(cf 4/16) (
Cartner et al, 1996). Infection
with larval
Echinococcus multilocularis by transportal injection
of hyatid homogenate results in a multivesiculation form of hyatid development
(cf 4/9) (
Nakaya et al, 1997). Susceptible
to
L. major mexicana, but vaccination against the parasite using
liposomes with parasite membrane antigens was not effective (contrast
CBA/Ca and C57BL/6) (Lazama-Davila, 1997).
Reproduction
C57BL/Fa
Poor reproductive performance (25/25) with only 3 young weaned per litter
and 0.4 young per female/week (Festing, 1976a).
C57BL/Ka
Good breeding performance, 2.2 young/female/month (6/24) (
Hansen et al., 1973., 1973).
C57BL/6
Good reproductive performance (3/8). Litter size 6.2 _ 0.2, sterility 8%
(
Nagasawa et al., 1973., 1973). Large
litter size (1/6), mean 6.2 (
Verley et al.,
1967., 1967). Good breeding performance, 2.5 young/female/month (2/24)
(
Hansen et al., 1973., 1973). Has longer
and more regular oestrus cycles than DBA/2 and C3H/HeJ (
Nelson et al 1992). Late opening of vagina and first cornification
(3/3), but early onset of cyclicity compared with C3H (
Nelson et al 1990).
Mice carrying the Y-chromosome from Mus musculus domesticus from
Tirano (Italy) or M.m. poschiavinus from Poschiavo (Switzerland)
fail to develop normal testes but instead develop ovaries and ovotestes.
Some hermaphroditic males become fertile, but the XY females lack normal
gonadal steroids and can not carry pregnancy to term. There is delayed
expression of IGF-I which may be responsible for the low setroid expression
(Villapandofierro et al, 1996).
C57BL/10
Good reproductive performance (3/25) with colony output 1.4 young/female/week,
litter size 6.9 (2/25) at weaning (Festing, 1976a). Intermediate breeding
performance (12/24) (
Hansen et al., 1973.,
1973).
Miscellaneous
C57BL/Ka
High degree of genetic distinctiveness (3/27) (
Taylor,
1972).
C57BL/6
High degree of genetic distinctiveness (4/27) (
Taylor,
1972). Recommended host for the following transplantable tumours:
mammary adenocarcinoma BW 10232 melanoma B16, myeloid leukaemia C 1498
and preputial gland carcinoma ESR586 (Kaliss, 1972).
Embryonic stem cell lines have been established (Kawase
et al, 1994).
High rate of spontaneous mutations at the agouti and W loci (1/21)
(Schlager and Dickie, 1967).
C57BL/10
High incidence of spontaneous `deviants' (possible mutants) (2/21) (
Schlager and Dickie, 1967).
C57BLKS.
Origin: C57BL/6J to Biesele in 1947, then pen bred, to Kaliss in 1948.
Ks resumed inbreeding. To J 1948. Differs from C57BL/6 and C57BL/10 at
the Bgls, Bglt, cdm and H2 loci as a result of a genetic
contamination, probably with a DBA substrain at the time the colony was
pen-bred. Resembles B6 at the Lv locus (at which B6 and B10 differ).
Formerly known as C57BL/Ks but renamed in Dec. 1994. Maint. by J.
Characteristics:
Low hepatic delta-aminolaevulinate dehydratase activity in Ks substrain
(7/8) (Doyle and Schimke, 1969). High susceptibility
to BALB/Tennant leukaemia virus in Ks substrain (3/12) (Tennant,
1965). Resistant to Herpes simplex virus (2/11) in Ks substrain
(Lopez, 1975). High retinal ganglion cell number
(22/24) (Williams et al, 1996).
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INBRED STRAINS OF MICE
Updated 9 Apr. 1998
Michael FW
Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,
UK
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