IMPC phenotypes (gene matching)
B6.129X1-Spo11tm1Mjn/Orl
| Status | Available to order |
| EMMA ID | EM:05730 |
| International strain name | B6.129X1-Spo11tm1Mjn/Orl |
| Alternative name | B.Cg-Spo11tm1Sky H2aw9/Orl ou Spo11_C57BL/6J |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Spo11tm1Mjn |
| Gene/Transgene symbol | Spo11 |
Information from provider
| Provider | Frederic BAUDAT |
| Provider affiliation | UPR1142 CNRS, Institut de Génétique Humaine |
| Genetic information | Exons 4 to 6 of Spo11 were replaced with a neomycin resistance cassette, removing the putative catalytic tyrosine encoded by exon 5. The Spo11 gene has been isolated from a 129/SvJ mouse genomic DNA library. A double-stranded linker containing the I-SceI recognition sequence was inserted at the NotI site of the vector pPNT, leading to the duplication of the NotI site. Then, a 2.1 kb HindIII/XbaI genomic fragment containing Spo11 exons 2 and 3 was inserted at the XbaI site. Finally, a 7.5 kb HindIII genomic fragment with exons 7-13 was inserted at the XhoI site of this intermediate, yielding the targeting vector pLSPR. |
| Phenotypic information | Homozygotes for the targeted null mutation are sterile. Mutant males exhibit loss of spermatocytes in early prophase, while mutant females exhibit oocyte loss soon after birth. |
| Breeding history | Knock-out construct introduced in 129X1 ES cells. Backcrossed with C57BL/6J for 11 generations. After that current inbreeding. |
| References |
|
| Homozygous fertile | no |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
| Animals used for archiving | heterozygous C57BL/6J, wild-type C57BL/6J |
Disease and phenotype information
MGI phenotypes (allele matching)
- small ovary / MGI
- abnormal meiosis / MGI
- decreased ovary weight / MGI
- abnormal female meiosis / MGI
- decreased oocyte number / MGI
- abnormal synaptonemal complex / MGI
- abnormal male meiosis / MGI
- arrest of male meiosis / MGI
- abnormal chromosomal synapsis / MGI
- abnormal double-strand DNA break repair / MGI
- abnormal ovary morphology / MGI
- impaired ovarian folliculogenesis / MGI
- small seminiferous tubules / MGI
- arrest of spermatogenesis / MGI
- abnormal spermatogenesis / MGI
- male infertility / MGI
- female infertility / MGI
- abnormal oogenesis / MGI
- decreased mature ovarian follicle number / MGI
- decreased testis weight / MGI
- azoospermia / MGI
- immune system phenotype / MGI
- abnormal spermatid morphology / MGI
- abnormal primordial ovarian follicle morphology / MGI
- oocyte degeneration / MGI
MGI phenotypes (gene matching)
- abnormal female reproductive system morphology / MGI
- abnormal ovary morphology / MGI
- small ovary / MGI
- impaired ovarian folliculogenesis / MGI
- absent mature ovarian follicles / MGI
- abnormal male reproductive system morphology / MGI
- small testis / MGI
- small seminiferous tubules / MGI
- arrest of spermatogenesis / MGI
- abnormal spermatogenesis / MGI
- male infertility / MGI
- female infertility / MGI
- abnormal gametogenesis / MGI
- abnormal meiosis / MGI
- abnormal oogenesis / MGI
- abnormal reproductive system morphology / MGI
- abnormal fertility/fecundity / MGI
- abnormal seminiferous tubule morphology / MGI
- decreased mature ovarian follicle number / MGI
- abnormal uterus development / MGI
- decreased testis weight / MGI
- decreased ovary weight / MGI
- azoospermia / MGI
- abnormal female meiosis / MGI
- abnormal male meiosis / MGI
- immune system phenotype / MGI
- decreased oocyte number / MGI
- abnormal spermatid morphology / MGI
- arrest of male meiosis / MGI
- early reproductive senescence / MGI
- oocyte degeneration / MGI
- abnormal primordial ovarian follicle morphology / MGI
- abnormal chromosomal synapsis / MGI
- abnormal synaptonemal complex / MGI
- abnormal double-strand DNA break repair / MGI
- abnormal X-Y chromosome synapsis during male meiosis / MGI
Literature references
- Chromosome synapsis defects and sexually dimorphic meiotic progression in mice lacking Spo11.;Baudat F, Manova K, Yuen J P, Jasin M, Keeney S, ;2000;Molecular cell;6;989-98; 11106739
- Recombinational DNA double-strand breaks in mice precede synapsis.;Mahadevaiah S K, Turner J M, Baudat F, Rogakou E P, de Boer P, Blanco-Rodríguez J, Jasin M, Keeney S, Bonner W M, Burgoyne P S, ;2001;Nature genetics;27;271-6; 11242108
- Distinct DNA-damage-dependent and -independent responses drive the loss of oocytes in recombination-defective mouse mutants.;Di Giacomo Monica, Barchi Marco, Baudat Frédéric, Edelmann Winfried, Keeney Scott, Jasin Maria, ;2005;Proceedings of the National Academy of Sciences of the United States of America;102;737-42; 15640358
- Surveillance of different recombination defects in mouse spermatocytes yields distinct responses despite elimination at an identical developmental stage.;Barchi Marco, Mahadevaiah Shantha, Di Giacomo Monica, Baudat Frédéric, de Rooij Dirk G, Burgoyne Paul S, Jasin Maria, Keeney Scott, ;2005;Molecular and cellular biology;25;7203-15; 16055729