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

Former Names 129/Sv-Dhhtm1Amc/J    (Changed: 15-DEC-04 ) Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse   Donating Investigator Andrew McMahon,   Harvard University

Description
Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous male mice are sterile due to arrested spermatogenesis at the late meiosis, primary spermatocyte stage. Female homozygotes are fertile. No gene product (mRNA) was detectable by semiquantitative RT-PCR analysis of peripheral nerve. Embryonic testis development is impaired. By six weeks of age, the mass of testes from homozygous males is 90% smaller than testes from heterozygous males. Histological examination reveals a diminished number of germ cells and no mature sperm in the testis or epididymis. Peripheral nerves from mutant mice appear flattened with structurally disorganized protective sheaths. The perineural cells, glia and mesenchymal cells, develop defective tight junctions, causing the perineurium to be permeable. This mutant mouse strain may be useful in studies related to male sterility and regulation of peripheral nerve development.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exons 1 and 2 and a portion of exon 3, which encode a conserved polypeptide required for protein activity. The construct was electroporated into 129S1/Sv-p⁺ Tyr⁺ Kitl^Sl-J/+ derived CJ7 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts.

Additional Web Information

New 129 Nomenclature Bulletin

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

46,xy Gonadal Dysgenesis, Partial, with Minifascicular Neuropathy - Models with phenotypic similarity to human disease where etiologies involve orthologs.1

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

Dhh^tm1Amc/Dhh^tm1Amc

        involves: 129S1/Sv * C57BL/6J

• endocrine/exocrine gland phenotype
• abnormal seminiferous tubule morphology
  • in most males, the seminiferous tubules were largely devoid of germ cells and contained only a residual lining of Sertoli cells   (MGI Ref ID J:57914)
  • notably, Leydig cells were present at 18.5 dpc but expression of patched homolog 1 was lost   (MGI Ref ID J:57914)
• • abnormal Sertoli cell morphology
    • only a residual lining of Sertoli cells was observed in most males   (MGI Ref ID J:57914)
• small testis
  • a progressive reduction in testicular mass was grossly evident at 18.5 dpc   (MGI Ref ID J:57914)
• reproductive system phenotype
• abnormal seminiferous tubule morphology
  • in most males, the seminiferous tubules were largely devoid of germ cells and contained only a residual lining of Sertoli cells   (MGI Ref ID J:57914)
  • notably, Leydig cells were present at 18.5 dpc but expression of patched homolog 1 was lost   (MGI Ref ID J:57914)
• • abnormal Sertoli cell morphology
    • only a residual lining of Sertoli cells was observed in most males   (MGI Ref ID J:57914)
• abnormal spermatogenesis
  • on a 129/Sv x C57BL/6J hybrid background, germ cells of some mice progressed through meiosis to late stages of spermiogenesis but sperm development was blocked at step 15; in contrast, on an inbred 129/Sv background, primary spermatocytes were formed but underwent cell death   (MGI Ref ID J:57914)
• • arrest of spermiogenesis
    • although step 15 spermatids were detected in tubules undergoing the transition from stage VI to stage VII, no step 16 spermatids were found in stage VII tubules, suggesting a developmental block at this stage   (MGI Ref ID J:57914)
  • azoospermia
    • no mature sperm were detected in the testis or epididymis   (MGI Ref ID J:57914)
• male infertility
  • male homozygotes were viable and displayed normal male anatomy and behavior but were infertile   (MGI Ref ID J:57914)
  • in contrast, female homozygotes were fully fertile   (MGI Ref ID J:57914)
• small testis
  • a progressive reduction in testicular mass was grossly evident at 18.5 dpc   (MGI Ref ID J:57914)

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

Dhh^tm1Amc/Dhh^tm1Amc

        involves: 129S1/Sv

• endocrine/exocrine gland phenotype
• abnormal seminiferous tubule morphology
  • in most males, the seminiferous tubules were largely devoid of germ cells and contained only a residual lining of Sertoli cells   (MGI Ref ID J:57914)
  • notably, Leydig cells were present at 18.5 dpc but expression of patched homolog 1 was lost   (MGI Ref ID J:57914)
• • abnormal Sertoli cell morphology
    • only a residual lining of Sertoli cells was observed in most males   (MGI Ref ID J:57914)
• small testis
  • at 18.5 dpc, homozygous mutant testes were grossly smaller than those of heterozygous littermates   (MGI Ref ID J:57914)
  • a progressive reduction in testicular mass was observed amounting to a 60% decrease at P10 and a 90% decrease at 6 weeks of age   (MGI Ref ID J:57914)
• reproductive system phenotype
• abnormal seminiferous tubule morphology
  • in most males, the seminiferous tubules were largely devoid of germ cells and contained only a residual lining of Sertoli cells   (MGI Ref ID J:57914)
  • notably, Leydig cells were present at 18.5 dpc but expression of patched homolog 1 was lost   (MGI Ref ID J:57914)
• • abnormal Sertoli cell morphology
    • only a residual lining of Sertoli cells was observed in most males   (MGI Ref ID J:57914)
• abnormal spermatid morphology
  • spermatids were not observed   (MGI Ref ID J:57914)
• arrest of spermatogenesis
  • on an inbred 129/Sv background, primary spermatocytes were formed but underwent cell death and no spermatids were observed; in contrast, on a 129/Sv x C57BL/6J hybrid background, germ cells of some mice progressed through meiosis to late stages of spermiprimary spermatocytes formed and underwent cell death ogenesis but sperm development was blocked at step 15   (MGI Ref ID J:57914)
• azoospermia
  • no mature sperm were detected in the testis or epididymis   (MGI Ref ID J:57914)
• male infertility
  • male homozygotes were viable and displayed normal male anatomy and behavior but were infertile   (MGI Ref ID J:57914)
  • in contrast, female homozygotes were fully fertile   (MGI Ref ID J:57914)
• small testis
  • at 18.5 dpc, homozygous mutant testes were grossly smaller than those of heterozygous littermates   (MGI Ref ID J:57914)
  • a progressive reduction in testicular mass was observed amounting to a 60% decrease at P10 and a 90% decrease at 6 weeks of age   (MGI Ref ID J:57914)

Dhh^tm1Amc/Dhh^tm1Amc

        involves: 129/Sv

• nervous system phenotype
• abnormal nervous system morphology
  • sciatic nerve flattened rather than round in cross-section   (MGI Ref ID J:57341)
  • little collagen in epineurium   (MGI Ref ID J:57341)
  • few fibroblasts in epineurium but perineurium-like cells present   (MGI Ref ID J:57341)
  • 2-4 layers in perineurium as opposed to 6-8 layers normally   (MGI Ref ID J:57341)
  • discontinuous basal lamina in perineurium   (MGI Ref ID J:57341)
  • cell junction defects between perineurium cells   (MGI Ref ID J:57341)
  • perineurial-like cells invade endoneurial space   (MGI Ref ID J:57341)
  • defective nerve tissue barrier, granulocyte invasion of nerves in inflammation   (MGI Ref ID J:57341)

Dhh^tm1Amc/Dhh^tm1Amc

        involves: 129S1/Sv * C57BL/6J * Swiss Webster

• endocrine/exocrine gland phenotype
• abnormal seminiferous tubule morphology
  • irregular and anastomotic tubules were observed in feminized adult males; tubular profiles were not rounded and the intertubular tissue displayed a few Leydig cells but extensive fibroblastic tissue   (MGI Ref ID J:65900)
  • relatively normal tubule appearance in masculinized adult males with small Sertoli cells and abundant adult-type Leydig cells in the interstitial lymphatic space   (MGI Ref ID J:65900)
• • abnormal Leydig cell morphology
    • masculinized adult males exhibited adult-type Leydig cells characterized by a dense cytoplasmic matrix, abundant smooth endoplasmic reticulum (SER), whorled ER, and a relative scarcity of lipid and glycogen, as well as an incomplete layer of parietal lymphatic endothelial cells external to the myoid cell layer   (MGI Ref ID J:65900)
    • in contrast, feminized males lacked both adult-type Leydig cells and a complete layer of parietal lymphatic endothelial cells; a few clusters of fetal-type Leydig cells were observed, with relatively less SER, a less dense cytoplasmic matrix compared to adult-type Leydig cells, no whorled SER, and abundant lipid and glycoge   (MGI Ref ID J:65900)
  • • Leydig cell hyperplasia
      • abundance of adult-type Leydig cells in the interstitial lymphatic space of masculinized males   (MGI Ref ID J:65900)
    • Leydig cell hypoplasia
      • significant reduction or near absence of adult-type Leydig cells in the interstitial testicular region of feminized males   (MGI Ref ID J:65900)
      • the relatively few Leydig cells that were present were identified as fetal based on their distinct morphology   (MGI Ref ID J:65900)
  • abnormal Sertoli cell morphology
    • in masculinized males, Sertoli cells were small and lacked a normal architecture in the relative absence of germ cells   (MGI Ref ID J:65900)
    • in feminized males, absence of a basement membrane resulted in apolar Sertoli cells   (MGI Ref ID J:65900)
  • abnormal peritubular myoid cell morphology
    • feminized males displayed immature myoid cells that were abnormally thickened instead of being flattened and lacked organized actin filaments and the pinocytotic vesicles observed in control testes   (MGI Ref ID J:65900)
    • in some cases, the myoid cell layer around the seminiferous tubules was discontinuous, with only collagen in the place of absent cells   (MGI Ref ID J:65900)
    • in some regions of feminized testes, the basement membrane between the myoid cell and cells of the seminiferous tubules was absent, whereas in other regions, the myoid cells gave rise to numerous microvilli that impinged upon the Sertoli cells   (MGI Ref ID J:65900)
  • • decreased number of peritubular myoid cells
      • at 20 days of age, no myoid cells or parietal lymphatic cells could be identified in feminized males   (MGI Ref ID J:65900)
      • in some cases where the basement membrane was absent, there was a direct intermingling of Leydig cells with Sertoli cells without any intervening peritubular tissue or extracellular basal laminae   (MGI Ref ID J:65900)
• abnormal testis cord formation
  • the basal lamina of seminiferous cords was not always continuous in newborn and adult mutant mice   (MGI Ref ID J:65900)
• cryptorchism
  • mutant testes were embedded in the fat pads in proximity to the kidneys   (MGI Ref ID J:65900)
• small testis
  • extremely reduced size of testes in both masculinized and feminized males   (MGI Ref ID J:65900)
  • testes of masculinized males were larger than those of feminized males   (MGI Ref ID J:65900)
• • decreased testis weight
    • the mean paired testis weight of feminized males was reduced to only 5% of that in heterozygous control mice   (MGI Ref ID J:65900)
• homeostasis/metabolism phenotype
• decreased circulating testosterone level
  • reduced levels of circulating testosterone in feminized males relative to controls (1.39 ± 0.05 ng/ml vs 3.6 ± 0.64 ng/ml, respectively)   (MGI Ref ID J:65900)
• increased circulating luteinizing hormone level
  • increased levels of circulating LH in feminized males relative to controls (14.1 ± 2.5 ng/ml vs 4.9 ± 1.0 ng/ml, respectively)   (MGI Ref ID J:65900)
  • normal serum levels of follicle stimulating hormone (FSH) in feminizied males relative to controls   (MGI Ref ID J:65900)
• reproductive system phenotype
• abnormal anogenital distance
  • masculinized males displayed a relatively longer urogenital-anal distance than feminized males   (MGI Ref ID J:65900)
• abnormal male germ cell morphology
  • in newborn (1-day-old) mice, germ cells were largely present within the seminiferous cords, but many were also found outside the cords   (MGI Ref ID J:65900)
  • no synaptonemal complexes were noted in extracordal germ cells, indicating that meiotic development had not occurred   (MGI Ref ID J:65900)
  • by 8 days of age, nearly all extracordal germ cells had been lost   (MGI Ref ID J:65900)
• • abnormal spermatocyte morphology
    • spermatogonia were evident but only a few spermatocytes were observed in masculinized adult males   (MGI Ref ID J:65900)
    • rare spermatocytes were observed in feminized adult males   (MGI Ref ID J:65900)
  • abnormal spermatogonia morphology
    • rare spermatogonia were observed in feminized adult males   (MGI Ref ID J:65900)
• abnormal seminiferous tubule morphology
  • irregular and anastomotic tubules were observed in feminized adult males; tubular profiles were not rounded and the intertubular tissue displayed a few Leydig cells but extensive fibroblastic tissue   (MGI Ref ID J:65900)
  • relatively normal tubule appearance in masculinized adult males with small Sertoli cells and abundant adult-type Leydig cells in the interstitial lymphatic space   (MGI Ref ID J:65900)
• • abnormal Leydig cell morphology
    • masculinized adult males exhibited adult-type Leydig cells characterized by a dense cytoplasmic matrix, abundant smooth endoplasmic reticulum (SER), whorled ER, and a relative scarcity of lipid and glycogen, as well as an incomplete layer of parietal lymphatic endothelial cells external to the myoid cell layer   (MGI Ref ID J:65900)
    • in contrast, feminized males lacked both adult-type Leydig cells and a complete layer of parietal lymphatic endothelial cells; a few clusters of fetal-type Leydig cells were observed, with relatively less SER, a less dense cytoplasmic matrix compared to adult-type Leydig cells, no whorled SER, and abundant lipid and glycoge   (MGI Ref ID J:65900)
  • • Leydig cell hyperplasia
      • abundance of adult-type Leydig cells in the interstitial lymphatic space of masculinized males   (MGI Ref ID J:65900)
    • Leydig cell hypoplasia
      • significant reduction or near absence of adult-type Leydig cells in the interstitial testicular region of feminized males   (MGI Ref ID J:65900)
      • the relatively few Leydig cells that were present were identified as fetal based on their distinct morphology   (MGI Ref ID J:65900)
  • abnormal Sertoli cell morphology
    • in masculinized males, Sertoli cells were small and lacked a normal architecture in the relative absence of germ cells   (MGI Ref ID J:65900)
    • in feminized males, absence of a basement membrane resulted in apolar Sertoli cells   (MGI Ref ID J:65900)
  • abnormal peritubular myoid cell morphology
    • feminized males displayed immature myoid cells that were abnormally thickened instead of being flattened and lacked organized actin filaments and the pinocytotic vesicles observed in control testes   (MGI Ref ID J:65900)
    • in some cases, the myoid cell layer around the seminiferous tubules was discontinuous, with only collagen in the place of absent cells   (MGI Ref ID J:65900)
    • in some regions of feminized testes, the basement membrane between the myoid cell and cells of the seminiferous tubules was absent, whereas in other regions, the myoid cells gave rise to numerous microvilli that impinged upon the Sertoli cells   (MGI Ref ID J:65900)
  • • decreased number of peritubular myoid cells
      • at 20 days of age, no myoid cells or parietal lymphatic cells could be identified in feminized males   (MGI Ref ID J:65900)
      • in some cases where the basement membrane was absent, there was a direct intermingling of Leydig cells with Sertoli cells without any intervening peritubular tissue or extracellular basal laminae   (MGI Ref ID J:65900)
• abnormal spermatogenesis
  • both masculinized (7.5%) and feminized (92.5%) males showed abnormal peritubular tissue and severely depressed spermatogenesis   (MGI Ref ID J:65900)
• • abnormal spermatocyte morphology
    • spermatogonia were evident but only a few spermatocytes were observed in masculinized adult males   (MGI Ref ID J:65900)
    • rare spermatocytes were observed in feminized adult males   (MGI Ref ID J:65900)
• abnormal testis cord formation
  • the basal lamina of seminiferous cords was not always continuous in newborn and adult mutant mice   (MGI Ref ID J:65900)
• cryptorchism
  • mutant testes were embedded in the fat pads in proximity to the kidneys   (MGI Ref ID J:65900)
• male infertility   (MGI Ref ID J:65900)
• male pseudohermaphroditism
  • 92.5% of mutant males were pseudohermaphrodites with an external female phenotype, evidence of mammary teats, and a blind vaginal opening; the remaining 7.5% mutant males were masculinized   (MGI Ref ID J:65900)
  • penetrance within the 92.5% varied; for example, some males were only partly feminized with colored teat hairs but lacking a blind vaginal opening   (MGI Ref ID J:65900)
  • internally, masculinized males were similar to feminized males except that the overall size of the reproductive tract was relatively larger, although still smaller, than that of wild-type or heterozygous controls   (MGI Ref ID J:65900)
• small testis
  • extremely reduced size of testes in both masculinized and feminized males   (MGI Ref ID J:65900)
  • testes of masculinized males were larger than those of feminized males   (MGI Ref ID J:65900)
• • decreased testis weight
    • the mean paired testis weight of feminized males was reduced to only 5% of that in heterozygous control mice   (MGI Ref ID J:65900)
• digestive/alimentary phenotype
• abnormal anogenital distance
  • masculinized males displayed a relatively longer urogenital-anal distance than feminized males   (MGI Ref ID J:65900)
• other phenotype
• fibrosis
  • feminized males show numerous layers of fibroblast-like cells with abundant intervening collagen external to the seminiferous tubules   (MGI Ref ID J:65900)
  • the fibrosis produced by the accumulation of collagen fibers in the interstitium of feminized testes increased with age   (MGI Ref ID J:65900)

View Research Applications

Research Applications

This mouse can be used to support research in many areas including:

Dhh^tm1Amc related

Developmental Biology Research
Internal/Organ Defects
      gonads
Neurodevelopmental Defects

Neurobiology Research
Neurodevelopmental Defects

Reproductive Biology Research
Fertility Defects
      males only

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Dhhtm1Amc
Allele Name		targeted mutation 1, Andrew P McMahon
Allele Type		Targeted (knock-out)
Common Name(s)		Dhh-;
Mutation Made By		Andrew McMahon,   Harvard University
Strain of Origin		129S1/Sv-Oca2<+> Tyr<+> Kitl<+>
ES Cell Line Name		CJ7
ES Cell Line Strain		129S1/Sv-Oca2<+> Tyr<+> Kitl<+>
Gene Symbol and Name		Dhh, desert hedgehog
Chromosome		15
Gene Common Name(s)		C78960; GDXYM; HHG-3; SRXY7; expressed sequence C78960;
Molecular Note		Exons 1, 2 and part of 3 were replaced with a neomycin cassette. The deleted segments encode a conserved polypeptide required for protein function. Thus, no functional protein is predicted to be produced from this allele. [MGI Ref ID J:57914]

Genotyping

Genotyping Information

Genotyping Protocols

Dhh^tm1Amc, Separated PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Bitgood MJ; Shen L; McMahon AP. 1996. Sertoli cell signaling by Desert hedgehog regulates the male germline. Curr Biol 6(3):298-304. [PubMed: 8805249]  [MGI Ref ID J:57914]

Additional References

Parmantier E; Lynn B; Lawson D; Turmaine M; Namini SS; Chakrabarti L; McMahon AP; Jessen KR; Mirsky R. 1999. Schwann cell-derived Desert hedgehog controls the development of peripheral nerve sheaths [see comments] Neuron 23(4):713-24. [PubMed: 10482238]  [MGI Ref ID J:57341]

Dhh^tm1Amc related

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]

Clark AM; Garland KK; Russell LD. 2000. Desert hedgehog (Dhh) gene is required in the mouse testis for formation of adult-type leydig cells and normal development of peritubular cells and seminiferous tubules Biol Reprod 63(6):1825-38. [PubMed: 11090455]  [MGI Ref ID J:65900]

Mirsky R; Parmantier E; McMahon AP; Jessen KR. 1999. Schwann cell-derived desert hedgehog signals nerve sheath formation. Ann N Y Acad Sci 883:196-202. [PubMed: 10586245]  [MGI Ref ID J:59851]

Park SY; Tong M; Jameson JL. 2007. Distinct roles for steroidogenic factor 1 and desert hedgehog pathways in fetal and adult Leydig cell development. Endocrinology 148(8):3704-10. [PubMed: 17495005]  [MGI Ref ID J:129625]

Parmantier E; Lynn B; Lawson D; Turmaine M; Namini SS; Chakrabarti L; McMahon AP; Jessen KR; Mirsky R. 1999. Schwann cell-derived Desert hedgehog controls the development of peripheral nerve sheaths [see comments] Neuron 23(4):713-24. [PubMed: 10482238]  [MGI Ref ID J:57341]

Pierucci-Alves F; Clark AM; Russell LD. 2001. A developmental study of the Desert hedgehog-null mouse testis. Biol Reprod 65(5):1392-402. [PubMed: 11673255]  [MGI Ref ID J:108687]

Sharghi-Namini S; Turmaine M; Meier C; Sahni V; Umehara F; Jessen KR; Mirsky R. 2006. The structural and functional integrity of peripheral nerves depends on the glial-derived signal desert hedgehog. J Neurosci 26(23):6364-76. [PubMed: 16763045]  [MGI Ref ID J:109214]

Umehara F; Mishima K; Egashira N; Ogata A; Iwasaki K; Fujiwara M. 2006. Elevated anxiety-like and depressive behavior in Desert hedgehog knockout male mice. Behav Brain Res 174(1):167-73. [PubMed: 16952407]  [MGI Ref ID J:112866]

Yao HH; Whoriskey W; Capel B. 2002. Desert Hedgehog/Patched 1 signaling specifies fetal Leydig cell fate in testis organogenesis. Genes Dev 16(11):1433-40. [PubMed: 12050120]  [MGI Ref ID J:82007]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.

Colony Maintenance

Breeding & Husbandry	The resulting mice were crossed at least once to C57BL/6, and have been maintained on a 129 background. The Donating Investigator maintains the strain by crossing homozygous females with heterozygous males. Homozygous males are sterile.

Purchasing information

Pricing, Supply Level & Notes, Controls

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• This strain is included in the Induced Mutant Resource Colony collection.

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The Jackson Laboratory's Genotype Promise

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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