IMPC phenotypes (allele matching)
B6;129S7-Cadm1tm1.2Brd/WtsiCnbc
| Status | Available to order |
| EMMA ID | EM:04806 |
| Citation information | RRID:IMSR_EM:04806 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | B6;129S7-Cadm1tm1.2Brd/WtsiCnbc |
| Alternative name | Tslc1-Brdm2 |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Cadm1tm1.2Brd |
| Gene/Transgene symbol | Cadm1 |
Information from provider
| Provider | Louise Van Der Weyden |
| Provider affiliation | Experimental Mouse Genetics, Wellcome Trust Sanger Institute |
| Genetic information | We have generated null allele of the Tslc1/Cadm1 gene by gene targeting. The targeted locus has loxP sites flanking exon 9 and FRT sites flanking the selection cassette. Exon 9 encodes the transmembrane domain (thus the exon 9-deleted form of the gene would not be membrane bound and would lack a functional cytoplasmic domain, and splicing of exon 8 with exon 10 would cause a shift in the reading frame). |
| Phenotypic information | Tslc1 null male mice were infertile. Tslc1 null adult testes showed that spermatogenesis had arrested at the spermatid stage, with degenerating and apoptotic spermatids sloughing off into the lumen. In adult mice, Tslc1 null round spermatids showed evidence of normal differentiation (an acrosomal cap and F-actin polarization indistinguishable from that of wild-type spermatids); however, the surviving spermatozoa were immature, malformed, found at very low levels in the epididymis, and rarely motile. Analysis of the first wave of spermatogenesis in Tslc1 null mice showed a delay in maturation by day 22 and degeneration of round spermatids by day 28. |
| Breeding history | Targeted ES cell clones (AB2.2) were transmitted through the germ line (chimaeric males bred to C57BL/6J females) and bred to homozygosity. Line maintained by interbreeding for at least 5 generations. Maintained on a mixed 129/Sv-C57BL/6 background. |
| References |
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| Homozygous fertile | no |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- abnormal hippocampus morphology / MGI
- arrest of spermatogenesis / MGI
- decreased body weight / MGI
- decreased body size / MGI
- abnormal tail movements / MGI
- male infertility / MGI
- abnormal T cell differentiation / MGI
- abnormal brain morphology / MGI
- no abnormal phenotype detected / MGI
- abnormal astrocyte morphology / MGI
- asthenozoospermia / MGI
- globozoospermia / MGI
- oligozoospermia / MGI
- nervous system phenotype / MGI
- increased pancreatic beta cell number / MGI
- decreased fetal size / MGI
- abnormal testis weight / MGI
- decreased testis weight / MGI
- decreased male germ cell number / MGI
- abnormal behavior / MGI
- increased double-positive T cell number / MGI
- decreased T cell proliferation / MGI
- endocrine/exocrine gland phenotype / MGI
- teratozoospermia / MGI
- abnormal spermatid morphology / MGI
- decreased CD4-positive, alpha beta T cell number / MGI
- decreased CD8-positive, alpha-beta T cell number / MGI
- arrest of spermiogenesis / MGI
- abnormal neocortex morphology / MGI
- decreased interferon-gamma secretion / MGI
- decreased interleukin-2 secretion / MGI
- decreased interleukin-4 secretion / MGI
- abnormal T cell receptor V(D)J recombination / MGI
- increased pancreatic beta cell mass / MGI
- short sperm flagellum / MGI
- multiflagellated sperm / MGI
- increased pancreatic beta cell proliferation / MGI
Literature references
- Loss of TSLC1 causes male infertility due to a defect at the spermatid stage of spermatogenesis.;van der Weyden Louise, Arends Mark J, Chausiaux Oriane E, Ellis Peter J, Lange Ulrike C, Surani M Azim, Affara Nabeel, Murakami Yoshinori, Adams David J, Bradley Allan, ;2006;Molecular and cellular biology;26;3595-609; 16611999