ATM Promotes RAD51-Mediated Meiotic DSB Repair by Inter-Sister-Chromatid Recombination in .

Meiotic recombination ensures accurate homologous chromosome segregation during meiosis and generates novel allelic combinations among gametes. During meiosis, DNA double strand breaks (DSBs) are generated to facilitate recombination. To maintain genome integrity, meiotic DSBs must be repaired using appropriate DNA templates. Although the DNA damage response protein kinase Ataxia-telangiectasia mutated (ATM) has been shown to be involved in meiotic recombination in , its mechanistic role is still unclear. In this study, we performed cytological analysis in mutant, we show that there are fewer γH2AX foci, but more RAD51 and DMC1 foci on meiotic chromosomes. Furthermore, we observed an increase in meiotic Type I crossovers (COs) in Our genetic analysis shows that the meiotic phenotype of double mutants is similar to the single mutant. Whereas, the double mutant has a more severe chromosome fragmentation phenotype compared to both single mutants, suggesting that ATM functions in concert with RAD51, but in parallel to DMC1. Lastly, we show that double mutants also have more severe meiotic recombination defects. These data lead us to propose a model wherein ATM promotes RAD51-mediated meiotic DSB repair by inter-sister-chromatid (IS) recombination in .