| First Author | Bannister LA | Year | 2007 |
| Journal | PLoS Biol | Volume | 5 |
| Issue | 5 | Pages | e105 |
| PubMed ID | 17425408 | Mgi Jnum | J:122037 |
| Mgi Id | MGI:3713019 | Doi | 10.1371/journal.pbio.0050105 |
| Citation | Bannister LA, et al. (2007) A dominant, recombination-defective allele of Dmc1 causing male-specific sterility. PLoS Biol 5(5):e105 |
| abstractText | DMC1 is a meiosis-specific homolog of bacterial RecA and eukaryotic RAD51 that can catalyze homologous DNA strand invasion and D-loop formation in vitro. DMC1-deficient mice and yeast are sterile due to defective meiotic recombination and chromosome synapsis. The authors identified a male dominant sterile allele of Dmc1, Dmc1(Mei11), encoding a missense mutation in the L2 DNA binding domain that abolishes strand invasion activity. Meiosis in male heterozygotes arrests in pachynema, characterized by incomplete chromosome synapsis and no crossing-over. Young heterozygous females have normal litter sizes despite having a decreased oocyte pool, a high incidence of meiosis I abnormalities, and susceptibility to premature ovarian failure. Dmc1(Mei11) exposes a sex difference in recombination in that a significant portion of female oocytes can compensate for DMC1 deficiency to undergo crossing-over and complete gametogenesis. Importantly, these data demonstrate that dominant alleles of meiosis genes can arise and propagate in populations, causing infertility and other reproductive consequences due to meiotic prophase I defects. |
