Large disruptions to mammalian spermatogenesis downstream of genetic perturbations in meiotic double-strand break repair
This study reveals that asymmetric PRDM9 binding in hybrid mice triggers asynapsis and meiotic silencing, leading to widespread fertility defects and aneuploidy, with individual sensitivity to these disruptions largely controlled by a specific locus on chromosome 15 containing Dmc1 and Mei1.