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.

交叉重组对于减数分裂染色体的分离至关重要，但是对哺乳动物如何完成交叉的了解却很少。在这里，我们通过分析Msh2 ^{– / –}错配校正缺陷所保留的重组分子中异源双链DNA的模式，阐明了雄性小鼠减数分裂重组过程中的链交换方式。突变体。令人惊讶的是，MSH2依赖的重组抑制并不明显。但是，很大一部分交换产物保留了异源双链DNA，有些提供了MSH2独立校正的证据。观察到有偏差的交叉拆分，与早期中间体中DNA末端之间的不对称一致。许多交换产物均未产生异源双链DNA，表明可通过D环迁移来拆除。与酵母中转换的复杂性不同，对原始双链断裂修复模型的这些简单修改（重组中间体的不对称性和D环迁移）可能足以解释小鼠中大多数减数分裂的转换，同时还解决了长期存在的相关问题到霍利迪交界处的分辨率。