Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N10F6pN1 Generation Definitions   Donating Investigator Eva Eicher,   The Jackson Laboratory

Development
The Nr0b1^tm1Lja floxed targeted mutation was generated in the mixed 129-derived ES cell line R1 and the resulting mice were bred with 129S1/SvImJ. This floxed allele arrived at The Jackson Laboratory on a primarily 129 background and was backcrossed once to C57BL/6J and then backcrossed repeatedly to C57BL/6JEi in the laboratory of Dr. Eva Eicher. This was then bred with C57BL/6J-Tg(Zp3-cre)93Knw to excise the floxed exon 2. The resulting Nr0b1^tm1.1Lja allele was backcrossed from a B6 background onto the DBA/2J background. On this DBA/2J background it proved possible to maintain the strain by breeding homozygous females with hemizygous males. In 2007 sperm were cryopreserved from hemizygous males at generation N10F6.

Related Strains

Strains carrying   Nr0b1^tm1.1Lja allele

006305

B6Ei.Cg-Nr0b1tm1.1Lja Tg(Sry)2Ei Chr YAKR/EiJ

View Strains carrying   Nr0b1^tm1.1Lja     (1 strain)

Strains carrying other alleles of Nr0b1

007006

B6Ei.129-Nr0b1tm1Lja/EiJ

View Strains carrying other alleles of Nr0b1     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Adrenal Hypoplasia, Congenital; AHC

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. 46,xy Sex Reversal 2; SRXY2   (NR0B1)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Nr0b1^tm1.1Lja/Nr0b1^tm1.1Lja

        involves: 129S1/Sv * 129X1/SvJ

• reproductive system phenotype
• polyovular ovarian follicle
  • subsets of follicles contain multiple oocytes   (MGI Ref ID J:51292)
  • however, female homozygotes are fertile, produce normal litter sizes, with no apparent defects in sexual maturation, ovarian formation or ovulation   (MGI Ref ID J:51292)
• endocrine/exocrine gland phenotype
• polyovular ovarian follicle
  • subsets of follicles contain multiple oocytes   (MGI Ref ID J:51292)
  • however, female homozygotes are fertile, produce normal litter sizes, with no apparent defects in sexual maturation, ovarian formation or ovulation   (MGI Ref ID J:51292)

Nr0b1^tm1.1Lja/Y

        involves: 129S1/Sv * 129X1/SvJ

• reproductive system phenotype
• abnormal spermatogenesis
  • spermatocytes are present at 10 weeks of age; however, germ cell depletion is observed at 14 weeks of age, indicating a defect in the maintenance of spermatogenesis   (MGI Ref ID J:51292)
• abnormal testis morphology
  • male hemizygotes display progressive loss of the germinal epithelium during postnatal testicular maturation   (MGI Ref ID J:51292)
• • abnormal Leydig cell morphology
    • at 12 weeks, Leydig cells in the interstitial space near the rete appear hyperplastic, with large mitochondria containing numerous tubular cristae   (MGI Ref ID J:71710)
    • in contrast, Leydig cells found in the seminiferous tubules are smaller and contain smaller mitochondria   (MGI Ref ID J:71710)
    • neither type of Leydig cell displays the cytoplasmic swirls of saccular endoplasmic reticulum typical of adult wild-type Leydig cells   (MGI Ref ID J:71710)
    • fetal Leydig cell development is arrested, with Leydig cells restricted to the ventral surface of the gonad   (MGI Ref ID J:81356)
  • • Leydig cell hyperplasia
      • at 10 weeks, interstitial Leydig cells show cellular hypertrophy and hyperplasia in the vicinity of severely degenerated seminiferous tubules   (MGI Ref ID J:51292)
      • at >1 yr of age, most male hemizygotes exhibit Leydig cell hyperplasia   (MGI Ref ID J:71710)
      • a few cases of Leydig cell neoplasia are also observed   (MGI Ref ID J:71710)
    • ectopic Leydig cells
      • at 12 weeks of age, seminiferous tubules close to the rete testis exhibit ectopic Leydig cells, distinct from the hyperplastic Leydig cells found in the interstitial space   (MGI Ref ID J:71710)
      • at 13.5 dpc, Leydig cells, which normally reside in the peritubular space and extend from the coelomic surface to the dorsal surface of the gonad, are restricted to the coelomic surface and almost completely excluded from the dorsal part of the gonad   (MGI Ref ID J:81356)
  • abnormal Sertoli cell development
    • at 13.5 dpc, organization and differentiation of mutant Sertoli cells is decreased relative to wild-type   (MGI Ref ID J:81356)
  • • Sertoli cell hyperplasia
      • at 12 weeks of age, abnormal proliferation of Sertoli cells results in the blockage of the rete testis and efferent ducts, impeding the passage of sperm into the epididymis   (MGI Ref ID J:71710)
  • abnormal efferent ductules of testis morphology
    • at 12 weeks of age, the proximal and middle efferent ductules are obstructed by Sertoli cells, blocking the passage of sperm, and the epithelium of the efferent duct is frequently overgrown   (MGI Ref ID J:71710)
    • notably, the epithelia display numerous basally positioned lipid deposits not observed in wild-type   (MGI Ref ID J:71710)
    • in contrast, the mutant epididymides appear morphologically normal   (MGI Ref ID J:71710)
  • abnormal peritubular myoid cell morphology
    • at 12 weeks of age, peritubular myoid cells appear poorly differentiated   (MGI Ref ID J:71710)
    • no basement membrane between the myoid cells and Sertoli cells is observed   (MGI Ref ID J:71710)
  • • decreased number of peritubular myoid cells
      • at 13.5 dpc, the number of peritubular myoid cells, which normally surround the testis cords, is reduced   (MGI Ref ID J:81356)
      • BrdU labeling of peritubular myoid cells is low, consistent with decreased proliferation   (MGI Ref ID J:81356)
  • abnormal seminiferous tubule epithelium morphology
    • at 10 weeks of age, some tubules display thin, irregular epithelia with sloughing of germ cells into the lumen   (MGI Ref ID J:51292)
    • occasional tubules show active spermatogenesis with stratified germinal epithelium and a relatively normal appearance   (MGI Ref ID J:51292)
    • at 12 weeks of age, vacuolation of the seminiferous epithelium and lipid accumulation are common in affected tubules, especially near the rete and in all tubules in older males, indicating a breakdown in Sertoli-germ cell junctions   (MGI Ref ID J:71710)
  • • ectopic Sertoli cells
      • at 12 weeks of age, the rete testis is blocked by ectopic Sertoli cells found within the lumen of the seminiferous tubules and efferent ducts   (MGI Ref ID J:71710)
  • abnormal testis cord formation
    • at 13.5 dpc, testis cord formation is delayed, as shown by a decreased number of cords that are poorly distinguished from the peritubular space   (MGI Ref ID J:81356)
    • at 13.5 dpc, the coelomic vessel is still present on the ventral surface; however, the ventral-dorsal width is intermediate between male and female gonads   (MGI Ref ID J:81356)
    • at 13.5 dpc, germ cells and Sertoli cells cluster together within the dorsal surface of the gonad, but only a few PTM cells are observed   (MGI Ref ID J:81356)
    • the basal lamina which defines the edges of individual testis cords is either disrupted or absent at 12.5, 13.5 and 14.5 dpc   (MGI Ref ID J:81356)
    • at 14.5 dpc, testis cord-like structures are present but appear smaller, irregular in shape, and with frequent breaks in laminin localization   (MGI Ref ID J:81356)
  • • disorganized testis cords
      • at 13.5 dpc, testis cords appear disorganized and incompletely formed; however, the number of germ and Sertoli cells and the expression of Sertoli-specific markers appear to be normal   (MGI Ref ID J:81356)
      • at 14.5 dpc, testis cords remain rudimentary, with occasional scattered PTM cells present at the ventral surface, leaving the dorsal half of the gonad more disorganized   (MGI Ref ID J:81356)
      • by 17.5 dpc, testis cords are larger than normal and more pleomorphic in shape, without clearly defined borders   (MGI Ref ID J:81356)
  • dilated seminiferous tubules
    • adult male hemizygotes exhibit dilated seminiferous tubules at all test ages   (MGI Ref ID J:71710)
    • tubule dilation is transient, with marked variability in the proportions of normal, dilated, and degenerating seminiferous tubules between different males of different ages   (MGI Ref ID J:71710)
  • rete testis obstruction
    • at 12 weeks of age, the rete testis is blocked by abnormally located Sertoli cells, creating a tailback of necrosing sperm in the testis   (MGI Ref ID J:71710)
  • seminiferous tubule degeneration
    • epithelial dysgenesis and degeneration exhibited at 10 weeks of age   (MGI Ref ID J:51292)
    • adult male hemizygotes exhibit degenerating seminiferous tubules at all test ages   (MGI Ref ID J:71710)
  • small testis
    • male hemizygotes have small testes despite normal serum levels of testosterone and gonadotropins   (MGI Ref ID J:51292)
  • • decreased testis weight
      • approximately 50% reduction in weight relative to wild-type   (MGI Ref ID J:51292)
      • at 12 weeks of age, mutant testes weigh significantly less than wild-type (126.2 ± 4.9 mg vs. 212.1 ± 18.0 mg, respectively)   (MGI Ref ID J:71710)
• absent germ cells
  • complete loss of male germ cells after 14 weeks of age   (MGI Ref ID J:51292)
• decreased male germ cell number
  • progressive loss of male germ cells evident at 10 weeks of age   (MGI Ref ID J:51292)
• male infertility
  • male hemizygotes display abnormal differentiation and proliferation of Leydig cells and Sertoli cells, leading to obstruction of the rete testis and infertility   (MGI Ref ID J:71710)
  • however, embryonic and early postnatal testosterone production is sufficient for formation of male internal and external genitalia and testicular descent however, testosterone production is sufficient for formation of male internal and external genitalia and testicular descent   (MGI Ref ID J:51292)
  • unlike female homozygotes, male hemizygotes are infertile   (MGI Ref ID J:51292)
• endocrine/exocrine gland phenotype
• *normal* endocrine/exocrine gland phenotype
  • normal zonae glomerulosa and fasciculata in adult cortical zones   (MGI Ref ID J:51292)
  • serum corticosterone levels were similar to those of wild-type mice, indicating normal adrenal secretion   (MGI Ref ID J:51292)
  • normal pituitary morphology   (MGI Ref ID J:51292)
  • normal serum levels of LH and FSH   (MGI Ref ID J:51292)
• • abnormal testis morphology
    • male hemizygotes display progressive loss of the germinal epithelium during postnatal testicular maturation   (MGI Ref ID J:51292)
  • • abnormal Leydig cell morphology
      • at 12 weeks, Leydig cells in the interstitial space near the rete appear hyperplastic, with large mitochondria containing numerous tubular cristae   (MGI Ref ID J:71710)
      • in contrast, Leydig cells found in the seminiferous tubules are smaller and contain smaller mitochondria   (MGI Ref ID J:71710)
      • neither type of Leydig cell displays the cytoplasmic swirls of saccular endoplasmic reticulum typical of adult wild-type Leydig cells   (MGI Ref ID J:71710)
      • fetal Leydig cell development is arrested, with Leydig cells restricted to the ventral surface of the gonad   (MGI Ref ID J:81356)
    • • Leydig cell hyperplasia
        • at 10 weeks, interstitial Leydig cells show cellular hypertrophy and hyperplasia in the vicinity of severely degenerated seminiferous tubules   (MGI Ref ID J:51292)
        • at >1 yr of age, most male hemizygotes exhibit Leydig cell hyperplasia   (MGI Ref ID J:71710)
        • a few cases of Leydig cell neoplasia are also observed   (MGI Ref ID J:71710)
      • ectopic Leydig cells
        • at 12 weeks of age, seminiferous tubules close to the rete testis exhibit ectopic Leydig cells, distinct from the hyperplastic Leydig cells found in the interstitial space   (MGI Ref ID J:71710)
        • at 13.5 dpc, Leydig cells, which normally reside in the peritubular space and extend from the coelomic surface to the dorsal surface of the gonad, are restricted to the coelomic surface and almost completely excluded from the dorsal part of the gonad   (MGI Ref ID J:81356)
    • abnormal Sertoli cell development
      • at 13.5 dpc, organization and differentiation of mutant Sertoli cells is decreased relative to wild-type   (MGI Ref ID J:81356)
    • • Sertoli cell hyperplasia
        • at 12 weeks of age, abnormal proliferation of Sertoli cells results in the blockage of the rete testis and efferent ducts, impeding the passage of sperm into the epididymis   (MGI Ref ID J:71710)
    • abnormal efferent ductules of testis morphology
      • at 12 weeks of age, the proximal and middle efferent ductules are obstructed by Sertoli cells, blocking the passage of sperm, and the epithelium of the efferent duct is frequently overgrown   (MGI Ref ID J:71710)
      • notably, the epithelia display numerous basally positioned lipid deposits not observed in wild-type   (MGI Ref ID J:71710)
      • in contrast, the mutant epididymides appear morphologically normal   (MGI Ref ID J:71710)
    • abnormal peritubular myoid cell morphology
      • at 12 weeks of age, peritubular myoid cells appear poorly differentiated   (MGI Ref ID J:71710)
      • no basement membrane between the myoid cells and Sertoli cells is observed   (MGI Ref ID J:71710)
    • • decreased number of peritubular myoid cells
        • at 13.5 dpc, the number of peritubular myoid cells, which normally surround the testis cords, is reduced   (MGI Ref ID J:81356)
        • BrdU labeling of peritubular myoid cells is low, consistent with decreased proliferation   (MGI Ref ID J:81356)
    • abnormal seminiferous tubule epithelium morphology
      • at 10 weeks of age, some tubules display thin, irregular epithelia with sloughing of germ cells into the lumen   (MGI Ref ID J:51292)
      • occasional tubules show active spermatogenesis with stratified germinal epithelium and a relatively normal appearance   (MGI Ref ID J:51292)
      • at 12 weeks of age, vacuolation of the seminiferous epithelium and lipid accumulation are common in affected tubules, especially near the rete and in all tubules in older males, indicating a breakdown in Sertoli-germ cell junctions   (MGI Ref ID J:71710)
    • • ectopic Sertoli cells
        • at 12 weeks of age, the rete testis is blocked by ectopic Sertoli cells found within the lumen of the seminiferous tubules and efferent ducts   (MGI Ref ID J:71710)
    • abnormal testis cord formation
      • at 13.5 dpc, testis cord formation is delayed, as shown by a decreased number of cords that are poorly distinguished from the peritubular space   (MGI Ref ID J:81356)
      • at 13.5 dpc, the coelomic vessel is still present on the ventral surface; however, the ventral-dorsal width is intermediate between male and female gonads   (MGI Ref ID J:81356)
      • at 13.5 dpc, germ cells and Sertoli cells cluster together within the dorsal surface of the gonad, but only a few PTM cells are observed   (MGI Ref ID J:81356)
      • the basal lamina which defines the edges of individual testis cords is either disrupted or absent at 12.5, 13.5 and 14.5 dpc   (MGI Ref ID J:81356)
      • at 14.5 dpc, testis cord-like structures are present but appear smaller, irregular in shape, and with frequent breaks in laminin localization   (MGI Ref ID J:81356)
    • • disorganized testis cords
        • at 13.5 dpc, testis cords appear disorganized and incompletely formed; however, the number of germ and Sertoli cells and the expression of Sertoli-specific markers appear to be normal   (MGI Ref ID J:81356)
        • at 14.5 dpc, testis cords remain rudimentary, with occasional scattered PTM cells present at the ventral surface, leaving the dorsal half of the gonad more disorganized   (MGI Ref ID J:81356)
        • by 17.5 dpc, testis cords are larger than normal and more pleomorphic in shape, without clearly defined borders   (MGI Ref ID J:81356)
    • dilated seminiferous tubules
      • adult male hemizygotes exhibit dilated seminiferous tubules at all test ages   (MGI Ref ID J:71710)
      • tubule dilation is transient, with marked variability in the proportions of normal, dilated, and degenerating seminiferous tubules between different males of different ages   (MGI Ref ID J:71710)
    • rete testis obstruction
      • at 12 weeks of age, the rete testis is blocked by abnormally located Sertoli cells, creating a tailback of necrosing sperm in the testis   (MGI Ref ID J:71710)
    • seminiferous tubule degeneration
      • epithelial dysgenesis and degeneration exhibited at 10 weeks of age   (MGI Ref ID J:51292)
      • adult male hemizygotes exhibit degenerating seminiferous tubules at all test ages   (MGI Ref ID J:71710)
    • small testis
      • male hemizygotes have small testes despite normal serum levels of testosterone and gonadotropins   (MGI Ref ID J:51292)
    • • decreased testis weight
        • approximately 50% reduction in weight relative to wild-type   (MGI Ref ID J:51292)
        • at 12 weeks of age, mutant testes weigh significantly less than wild-type (126.2 ± 4.9 mg vs. 212.1 ± 18.0 mg, respectively)   (MGI Ref ID J:71710)
  • retention of the x-zone
    • retention of fetal X-zone   (MGI Ref ID J:51292)
• tumorigenesis
• testis tumor
  • at >1 year of age, approximately 1/3 of male hemizygotes display bilateral testicular tumors, immunohistochemically confirmed as sex cord-stromal and not germ cell in origin   (MGI Ref ID J:71710)
  • these tumors are either derived from cells of the Sertoli/granulosa cell lineage or Leydig interstitial cells   (MGI Ref ID J:71710)
  • in both cases, the tumors cause tubular degeneration and a block of spermatogenesis and are mitotically active   (MGI Ref ID J:71710)
  • typically, the surrounding testicular tissue is composed of hemorrhage and fluid   (MGI Ref ID J:71710)
• homeostasis/metabolism phenotype
• abnormal lipid homeostasis
  • at 12 weeks of age, male hemizygotes show significant lipid deposits in the interstitial tissue immediately adjacent to the blockage of rete testis by Sertoli cells   (MGI Ref ID J:71710)
  • many of the macrophages observed in interstitial tissue contain cholesterol crystalloid structures   (MGI Ref ID J:71710)
  • cholesterol crystals are also noted in several Leydig and Sertoli cells, suggesting a steroidogenic defect   (MGI Ref ID J:71710)
  • in addition, the epithelium of the efferent duct contains numerous basally positioned lipid deposits not observed in wild-type controls   (MGI Ref ID J:71710)

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Nr0b1tm1.1Lja
Allele Name		targeted mutation 1.1, J Larry Jameson
Allele Type		Targeted (knock-out)
Common Name(s)		Ahchdelta2; Dax1-; Dax1KO;
Mutation Made By		Linda Washburn,   The Jackson Laboratory
Strain of Origin		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line Name		R1
ES Cell Line Strain		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name		Nr0b1, nuclear receptor subfamily 0, group B, member 1
Chromosome		X
Gene Common Name(s)		AHC; AHCH; AHX; Ahc; Ahch; DAX-1; DAX1; DSS; GTD; HHG; NROB1; SRXY2; adrenal hypoplasia, congenital; adrenal hypoplasia, congenital homolog (human);
Molecular Note		This allele is a derivative of Nr0b1tm1Lja in which Cre-mediated recombination in vivo under control of a CMV promoter excised exon 2 in the germline. RT-PCR analyses of pituitary, adrenal glands, and gonads did not detect full length transcript in either homozygous female mice or hemizygous male mice. [MGI Ref ID J:51292]

Genotyping

Genotyping Information

Genotyping Protocols

Nr0b1^{tm1Lja, tm1.1Lja}, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Bouma GJ; Albrecht KH; Washburn LL; Recknagel AK; Churchill GA; Eicher EM. 2005. Gonadal sex reversal in mutant Dax1 XY mice: a failure to upregulate Sox9 in pre-Sertoli cells. Development 132(13):3045-54. [PubMed: 15944188]  [MGI Ref ID J:98922]

Additional References

Nr0b1^tm1.1Lja related

Achermann JC; Meeks JJ; Larry Jameson J. 2001. Phenotypic spectrum of mutations in DAX-1 and SF-1. Mol Cell Endocrinol 185(1-2):17-25. [PubMed: 11738790]  [MGI Ref ID J:73634]

Babu PS; Bavers DL; Beuschlein F; Shah S; Jeffs B; Jameson JL; Hammer GD. 2002. Interaction between Dax-1 and steroidogenic factor-1 in vivo: increased adrenal responsiveness to ACTH in the absence of Dax-1. Endocrinology 143(2):665-73. [PubMed: 11796523]  [MGI Ref ID J:74975]

Brennan J; Capel B. 2004. One tissue, two fates: molecular genetic events that underlie testis versus ovary development. Nat Rev Genet 5(7):509-21. [PubMed: 15211353]  [MGI Ref ID J:90770]

Jeffs B; Ito M; Yu RN; Martinson FA; Wang ZJ; Doglio LT; Jameson JL. 2001. Sertoli cell-specific rescue of fertility, but not testicular pathology, in Dax1 (Ahch)-deficient male mice. Endocrinology 142(6):2481-8. [PubMed: 11356697]  [MGI Ref ID J:70206]

Jeffs B; Meeks JJ; Ito M; Martinson FA; Matzuk MM; Jameson JL; Russell LD. 2001. Blockage of the rete testis and efferent ductules by ectopic sertoli and leydig cells causes infertility in dax1-deficient male mice. Endocrinology 142(10):4486-95. [PubMed: 11564714]  [MGI Ref ID J:71710]

Kopp P. 1999. Targeted disruption of the Ahch (Dax-1) gene: knockout of old concepts. Eur J Endocrinol 140(4):291-2. [PubMed: 10097246]  [MGI Ref ID J:54550]

Martin LJ; Tremblay JJ. 2010. Nuclear receptors in leydig cell gene expression and function. Biol Reprod 83(1):3-14. [PubMed: 20375256]  [MGI Ref ID J:161974]

Meeks JJ; Crawford SE; Russell TA; Morohashi K; Weiss J; Jameson JL. 2003. Dax1 regulates testis cord organization during gonadal differentiation. Development 130(5):1029-36. [PubMed: 12538527]  [MGI Ref ID J:81356]

Meeks JJ; Russell TA; Jeffs B; Huhtaniemi I; Weiss J; Jameson JL. 2003. Leydig cell-specific expression of DAX1 improves fertility of the Dax1-deficient mouse. Biol Reprod 69(1):154-60. [PubMed: 12606353]  [MGI Ref ID J:84030]

Meeks JJ; Weiss J; Jameson JL. 2003. Dax1 is required for testis determination. Nat Genet 34(1):32-3. [PubMed: 12679814]  [MGI Ref ID J:83187]

Park SY; Lee EJ; Emge D; Jahn CL; Jameson JL. 2008. A phenotypic spectrum of sexual development in Dax1 (Nr0b1)-deficient mice: consequence of the C57BL/6J strain on sex determination. Biol Reprod 79(6):1038-45. [PubMed: 18633137]  [MGI Ref ID J:145808]

Park SY; Meeks JJ; Raverot G; Pfaff LE; Weiss J; Hammer GD; Jameson JL. 2005. Nuclear receptors Sf1 and Dax1 function cooperatively to mediate somatic cell differentiation during testis development. Development 132(10):2415-23. [PubMed: 15829514]  [MGI Ref ID J:98517]

Scheys JO; Heaton JH; Hammer GD. 2011. Evidence of adrenal failure in aging Dax1-deficient mice. Endocrinology 152(9):3430-9. [PubMed: 21733829]  [MGI Ref ID J:176895]

Wang ZJ; Jeffs B; Ito M; Achermann JC; Yu RN; Hales DB; Jameson JL. 2001. Aromatase (Cyp19) expression is up-regulated by targeted disruption of Dax1. Proc Natl Acad Sci U S A 98(14):7988-93. [PubMed: 11427738]  [MGI Ref ID J:191932]

Yu RN; Ito M; Saunders TL; Camper SA; Jameson JL. 1998. Role of Ahch in gonadal development and gametogenesis [see comments] Nat Genet 20(4):353-7. [PubMed: 9843206]  [MGI Ref ID J:51292]

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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