Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis
Regulating double-stranded DNA break repair towards crossover or non-crossover during mammalian meiosis
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DOI：
10.1007/s10577-007-1140-3
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发表时间：
2007-01-01
影响因子：
2.6
通讯作者：
de Massy, Bernard
中科院分区：
文献类型：
--
作者：
Baudat, Frederic;de Massy, Bernard
在减数分裂过程中，DNA 双链断裂 (DSB) 的程序化诱导导致交叉 (CO) 和非交叉产物 (NCO)。 CO 的一个关键作用是在中期 I 之前连接同系物，从而确保适当的还原分离。这一作用意味着通过在每个染色体臂上建立至少一个 CO 来精确调节 CO 频率。当前的主要挑战是了解 CO 和 NCO 的形成如何受到监管以及 NCO 的作用是什么。我们在此介绍关于 CO 和 NCO 及其在哺乳动物中的调节的最新知识。 CO 密度沿染色体变化很大，并且它们的分布不是随机的，因为它们会受到正干扰。正如在小鼠和人类中所记录的那样，相对于 CO 的数量，产生了显着过量的 DSB。事实上，已经获得了 NCO 产物形成、针对 CO 或 NCO 的 DSB 修复选择的调节以及 CO 特异性途径的证据。我们讨论了 Msh4、Msh5 和 Sycp1 的作用，它们影响 DSB 修复，而且可能不仅影响 CO 途径。我们认为，在哺乳动物中，NCO 的调节与酿酒酵母中描述的不同。
During meiosis the programmed induction of DNA double-stranded breaks (DSB) leads to crossover (CO) and non-crossover products (NCO). One key role of CO is to connect homologs before metaphase I and thus to ensure the proper reductional segregation. This role implies an accurate regulation of CO frequency with the establishment of at least one CO per chromosome arm. Current major challenges are to understand how CO and NCO formation are regulated and what is the role of NCO. We present here the current knowledge about CO and NCO and their regulation in mammals. CO density varies widely along chromosomes and their distribution is not random as they are subject to positive interference. As documented in the mouse and human, a significant excess of DSB are generated relative to the number of CO. In fact, evidence has been obtained for the formation of NCO products, for regulation of the choice of DSB repair towards CO or NCO and for a CO specific pathway. We discuss the roles of Msh4, Msh5 and Sycp1 which affect DSB repair and probably not only the CO pathway. We suggest that, in mammals, the regulation of NCO differs from that described in Saccharomyces cerei4siac.