Abstract: |
Crossover recombination is critical for meiotic chromosome segregation, but how mammalian crossing over is accomplished is poorly understood. Here, we illuminate how strands exchange during meiotic recombination in male mice by analyzing patterns of heteroduplex DNA in recombinant molecules preserved by the mismatch correction deficiency of Msh2–/– mutants. Surprisingly, MSH2-dependent recombination suppression was not evident. However, a substantial fraction of crossover products retained heteroduplex DNA, and some provided evidence of MSH2-independent correction. Biased crossover resolution was observed, consistent with asymmetry between DNA ends in earlier intermediates. Many crossover products yielded no heteroduplex DNA, suggesting dismantling by D-loop migration. Unlike the complexity of crossovers in yeast, these simple modifications of the original double-strand break repair model—asymmetry in recombination intermediates and D-loop migration—may be sufficient to explain most meiotic crossing over in mice while also addressing long-standing questions related to Holliday junction resolution. © 2020 Elsevier Inc. Crossover formation is essential for gamete viability, yet our understanding of mammalian mechanisms largely relies on inference from yeast. Peterson et al. illuminate mechanisms of crossover formation, including commonalities with yeast while distinguishing mammalian-specific differences. This fine-scale study of recombination intermediates allowed revision of the canonical model of crossover formation in mice. © 2020 Elsevier Inc. |