During meiosis, a molecular program induces DNA double-strand breaks (DSBs) and their repair by homologous recombination. DSBs can be repaired with or without crossovers. ZMM proteins promote the repair toward crossover. The sites of DSB repair are also sites where the axes of homologous chromosomes are juxtaposed and stabilized, and where a structure called the synaptonemal complex initiates, providing further regulation of both DSB formation and repair. How crossover formation and synapsis initiation are linked has remained unknown. The study by Pyatnitskaya and colleagues (pp. 53–69) in this issue of Genes & Development highlights the central role of the Saccharomyces cerevisiae ZMM protein Zip4 in this process.

中文翻译：

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减数分裂中的耦合交叉和联会复合体

在减数分裂期间，分子程序诱导 DNA 双链断裂 (DSB) 并通过同源重组对其进行修复。DSB 可以在有或没有分频器的情况下进行修复。ZMM 蛋白促进对交叉的修复。DSB 修复位点也是同源染色体的轴并列并稳定的位点，也是称为联会复合体的结构起始的位点，提供了对 DSB 形成和修复的进一步调节。交叉形成和突触起始如何联系仍然未知。Pyatnitskaya 及其同事（第 53-69 页）在本期《基因与发展》中的研究强调了酿酒酵母ZMM 蛋白 Zip4 在这一过程中的核心作用。