| 69716 | Q3UA06 | PCH2_MOUSE | Pachytene checkpoint protein 2 homolog (Thyroid hormone receptor interactor 13) (Thyroid receptor-interacting protein 13) (TR-interacting protein 13) (TRIP-13) | DISRUPTION PHENOTYPE | Mice develop normally without obvious somatic defects but males and females are sterile due to meiotic disruption in meiocytes. Homozygous mutants display small gonads and females have few or no follicles, due to oocyte elimination between pachynema and dictyate. Mutant testes display reduced populated tubules and spermatogenesis is mainly arrested at spermatocyte stages of epithelial stage IV, corresponding to pachynema. Different phenotypes are observed in the different knockout experiments tested. In Trip13(RRB047) mutant mice, also named Trip13(mod) allele for moderate, the number of crossovers are not affected and meiocytes undergo homologous chromosome synapsis despide the presence of unrepaired DSBs in pachynema. Using a more severe mutant allele, named Trip13(sev) for severe, additional defects are observed: the numbers of crossovers and chiasmata are reduced in the absence of TRIP13, and their distribution along the chromosomes is altered (PubMed:20711356). Autosomal bivalents in meiocytes frequently display pericentric synaptic forks and other defects (PubMed:20711356). Recombination defects are evident very early in meiotic prophase, soon after DSB formation (PubMed:20711356). These results suggest that the absence of defects in the number of crossovers observed in Trip13(RRB047) mutant is due to the use of a weak hypomorphic mutant allele. {ECO:0000269|PubMed:17696610, ECO:0000269|PubMed:20711356}. |