Institut de Génétique Humaine (IGH), Centre National de la Recherche Scientifique, Université Montpellier, Montpellier 34396, France.
Genes Dev. 2022 Jan 1;36(1-2):4-6. doi: 10.1101/gad.349286.121.
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 highlights the central role of the ZMM protein Zip4 in this process.
在减数分裂过程中,一个分子程序诱导 DNA 双链断裂 (DSB) 及其同源重组修复。DSB 可以不发生交叉而修复,也可以发生交叉而修复。ZMM 蛋白促进向交叉修复的进行。DSB 修复的部位也是同源染色体轴并列和稳定的部位,在这里会起始一个叫做联会复合体的结构,进一步调节 DSB 的形成和修复。交叉形成和联会起始是如何联系在一起的仍然未知。Pyatnitskaya 及其同事在本期杂志上的研究(第 53-69 页)强调了 ZMM 蛋白 Zip4 在这个过程中的核心作用。