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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Cga-cre)3Sac
transgene insertion 3, Sally A Camper
MGI:2179995
Summary 7 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Nr5a1tm2Klp/Nr5a1tm2.1Klp
Tg(Cga-cre)3Sac/0
involves: 129P2/OlaHsd * C57BL/6J * SJL MGI:2180104
cn2
Nr5a1tm2Klp/Nr5a1tm2Klp
Tg(Cga-cre)3Sac/0
involves: 129P2/OlaHsd * C57BL/6J * SJL MGI:2180121
cn3
Gata2tm1Sac/Gata2tm1Sac
Tg(Cga-cre)3Sac/?
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL MGI:3639705
cn4
Esr1tm1.2Mma/Esr1tm1.2Mma
Tg(Cga-cre)3Sac/0
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL MGI:3798388
cn5
Bmpr1atm1Bhr/Bmpr1atm2.1Bhr
Tg(Cga-cre)3Sac/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:3819176
cn6
Dio2tm1Acb/Dio2tm1Acb
Tg(Cga-cre)3Sac/0
involves: C57BL/6J * SJL MGI:5513867
cn7
Foxl2tm2.1Tre/Foxl2tm2.1Tre
Tg(Cga-cre)3Sac/0
involves: C57BL/6 * SJL MGI:4430333


Genotype
MGI:2180104
cn1
Allelic
Composition
Nr5a1tm2Klp/Nr5a1tm2.1Klp
Tg(Cga-cre)3Sac/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr5a1tm2.1Klp mutation (0 available); any Nr5a1 mutation (30 available)
Nr5a1tm2Klp mutation (2 available); any Nr5a1 mutation (30 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic prostate glands
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic seminal vesicles
• although ovarian follicles develop through the primary, secondary and antral stages, no large preovulatory follicles or corpora lutea are observed
• treatment with exogenous gonadotropins (PMSG) stimulated maturation of ovarian follicles to the preovulatory stage and induced ovulation, as indicated by the presence of corpora lutea
• severe
• mutant Leydig cells display none of the histological features typical of steroidogenic cells
• interstitial Leydig cells are severely reduced in number
• treatment with exogenous gonadotropins stimulated Leydig cell hypertrophy and induced luminal opening of the seminiferous tubules
• severe
• mutant males have cryptorchid testes

reproductive system
• male germ cells are significantly reduced in number
• although ovarian follicles develop through the primary, secondary and antral stages, no large preovulatory follicles or corpora lutea are observed
• treatment with exogenous gonadotropins (PMSG) stimulated maturation of ovarian follicles to the preovulatory stage and induced ovulation, as indicated by the presence of corpora lutea
• treatment with exogenous gonadotropins (PMSG) stimulated a significant increase in uterine size and development of the endometrial glands
• mutant males fail to progress through the normal stages of spermatogenesis: occasional pachytene spermatocytes are observed, but mature spermatids are absent
• treatment with exogenous gonadotropins (PMSG) stimulated gonadal steroidogenesis, inducing maturation of spermatogonial precursors to the round spermatid stage
• no mature spermatids are observed
• mutant males show hypoplastic external and internal genitalia
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic prostate glands
• treatment with exogenous gonadotropins stimulated enlargement of the hypoplastic seminal vesicles
• mutant Leydig cells display none of the histological features typical of steroidogenic cells
• interstitial Leydig cells are severely reduced in number
• treatment with exogenous gonadotropins stimulated Leydig cell hypertrophy and induced luminal opening of the seminiferous tubules
• mutant males have cryptorchid testes
• mutant gonads are severely hypoplastic
• severe
• severe
• mutant vaginas fail to open at the normal age of puberty
• both male and female mutants are viable but fail to show signs of secondary sexual maturation, even at 6 months of age
• both male and female mutants exhibit sexual infantilism of the accessory sex organs

homeostasis/metabolism
• although mutant pituitaries appear histologically intact, immunoreactive FSH leves are virtually undetectable
• in contrast, pituitary ACTH, TSH and prolactin levels are comparable to those in wild-type pituitaries
• serum FSH levels are significantly reduced in both male and female mutants relative to wild-type controls
• although mutant pituitaries appear histologically intact, immunoreactive LH leves are virtually undetectable
• serum LH levels are significantly reduced in male mutants relative to wild-type controls

cellular
• no mature spermatids are observed
• male germ cells are significantly reduced in number

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
hypogonadotropic hypogonadism DOID:0090070 OMIM:PS147950
J:66593




Genotype
MGI:2180121
cn2
Allelic
Composition
Nr5a1tm2Klp/Nr5a1tm2Klp
Tg(Cga-cre)3Sac/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nr5a1tm2Klp mutation (2 available); any Nr5a1 mutation (30 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• similar to that observed in mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• similar to that observed in mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• neither large preovulatory follicles nor corpora lutea are observed, similar to mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• mutant mice display absence of follicular maturation beyond the antral stage
• although mutant ovaries are smaller than wild-type, they are significantly larger than those of mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• at 8 weeks of age, the weight of mutant ovaries (0.06 g/kg) is significantly lower than wild-type (0.47 g/kg), but higher than that of mice which are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac (0.01 g/kg)
• at 8 weeks of age, mutant interstitial Leydig cells are severely hypoplastic
• in contrast, Sertoli cells and developing germ cells (including mature sperm) are relatively intact
• although mutant testes are smaller than wild-type, they are significantly larger than those of mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• at 8 weeks of age, the weight of mutant testes (3.7 g/kg) is significantly lower than wild-type (7.9 g/kg), but significantly higher than that of mice which are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac (0.4 g/kg)
• similar to that observed in mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• both male and female mutants show a milder degree of (hypomorphic) hypogonadism than mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• both male and female mutants show little evidence for secondary sexual maturation

endocrine/exocrine glands
• similar to that observed in mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• similar to that observed in mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• neither large preovulatory follicles nor corpora lutea are observed, similar to mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• mutant mice display absence of follicular maturation beyond the antral stage
• although mutant ovaries are smaller than wild-type, they are significantly larger than those of mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• at 8 weeks of age, the weight of mutant ovaries (0.06 g/kg) is significantly lower than wild-type (0.47 g/kg), but higher than that of mice which are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac (0.01 g/kg)
• at 8 weeks of age, mutant interstitial Leydig cells are severely hypoplastic
• in contrast, Sertoli cells and developing germ cells (including mature sperm) are relatively intact
• although mutant testes are smaller than wild-type, they are significantly larger than those of mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac
• at 8 weeks of age, the weight of mutant testes (3.7 g/kg) is significantly lower than wild-type (7.9 g/kg), but significantly higher than that of mice which are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac (0.4 g/kg)

homeostasis/metabolism
• mutant mice of both sexes show circulating FSH levels (4.5 ng/ml males, 5.2 ng/ml females) that are intermediate between those of wild-type mice (31.35 ng/ml males, 12.4 ng/ml females) and mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac (1.2 ng/ml males, 2.7 ng/ml females)
• mutant males display a severe reduction in circulating LH levels similar to that observed in mice that are heterozygous for Nr5a1tm2Klp and Nr5a1tm2.1Klp and hemizygous for Tg(Cga-cre)3Sac

behavior/neurological
• mutants do not engage in sexual activity




Genotype
MGI:3639705
cn3
Allelic
Composition
Gata2tm1Sac/Gata2tm1Sac
Tg(Cga-cre)3Sac/?
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata2tm1Sac mutation (1 available); any Gata2 mutation (30 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• fewer thyrotrope and gonadotrope in neonates
• thyrotrope population recover in adult
• weights approximately 55% that of wild-type
• inability to increases TSH production and secretion in response to severe hypothyroidism induced by radiothyroidectomy

nervous system
• fewer thyrotrope and gonadotrope in neonates
• thyrotrope population recover in adult
• inability to increases TSH production and secretion in response to severe hypothyroidism induced by radiothyroidectomy

homeostasis/metabolism
• in the male at 56% the level of wild-type

reproductive system
• weights approximately 55% that of wild-type

growth/size/body
• beginning at 3 weeks of age, the male mutant begin to show growth insufficiency




Genotype
MGI:3798388
cn4
Allelic
Composition
Esr1tm1.2Mma/Esr1tm1.2Mma
Tg(Cga-cre)3Sac/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Esr1tm1.2Mma mutation (0 available); any Esr1 mutation (68 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• occasionally follicular cysts are observed in mice
• irregular cycling

endocrine/exocrine glands
• occasionally follicular cysts are observed in mice

growth/size/body
• occasionally follicular cysts are observed in mice




Genotype
MGI:3819176
cn5
Allelic
Composition
Bmpr1atm1Bhr/Bmpr1atm2.1Bhr
Tg(Cga-cre)3Sac/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmpr1atm1Bhr mutation (1 available); any Bmpr1a mutation (90 available)
Bmpr1atm2.1Bhr mutation (1 available); any Bmpr1a mutation (90 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• occurs at E12.5 likely due to heart defects

embryo
• embryos are smaller than wild-type littermates at prior to lethality

growth/size/body
• embryos are smaller than wild-type littermates at prior to lethality

endocrine/exocrine glands
• at E10.5 pouch is thin and underdeveloped compared to wild-type littermates

nervous system
• at E10.5 pouch is thin and underdeveloped compared to wild-type littermates

cardiovascular system
• embryos display heart defects




Genotype
MGI:5513867
cn6
Allelic
Composition
Dio2tm1Acb/Dio2tm1Acb
Tg(Cga-cre)3Sac/0
Genetic
Background
involves: C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dio2tm1Acb mutation (0 available); any Dio2 mutation (19 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• mice treated with T4 exhibit a lower reduction in serum TSH likely due to impaired T4 to T3 conversion compared with control mice
• with elevated free T4 levels

adipose tissue

endocrine/exocrine glands
N
• mice are systematically euthyroid




Genotype
MGI:4430333
cn7
Allelic
Composition
Foxl2tm2.1Tre/Foxl2tm2.1Tre
Tg(Cga-cre)3Sac/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Foxl2tm2.1Tre mutation (0 available); any Foxl2 mutation (15 available)
Tg(Cga-cre)3Sac mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• almost entire structure is affected
• instead of normal granulosa cells, cells with morphological characteristics of Sertoli cells (prominent basal lamina, tripartite nuclei, numerous veil-like cytoplasmic extensions pointing toward lumen) are observed
• typical follicular structure of ovary resembles seminiferous tubules of testis
• size is increased compared to control females
• female mice exhibit gonadal sex reversal

endocrine/exocrine glands
• almost entire structure is affected
• instead of normal granulosa cells, cells with morphological characteristics of Sertoli cells (prominent basal lamina, tripartite nuclei, numerous veil-like cytoplasmic extensions pointing toward lumen) are observed
• typical follicular structure of ovary resembles seminiferous tubules of testis
• size is increased compared to control females





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory