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首页> 美国卫生研究院文献>Nucleic Acids Research >A pathway for error-free non-homologous end joining of resected meiotic double-strand breaks
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A pathway for error-free non-homologous end joining of resected meiotic double-strand breaks

机译：用于切除的减排的减排的减数分子双链断裂的无差无关的轨道途径

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摘要

Programmed DNA double-strand breaks (DSBs) made during meiosis are repaired by recombination with the homologous chromosome to generate, at selected sites, reciprocal crossovers that are critical for the proper separation of homologs in the first meiotic division. Backup repair processes can compensate when the normal meiotic recombination processes are non-functional. We describe a novel backup repair mechanism that occurs when the homologous chromosome is not available in Drosophila melanogaster meiosis. In the presence of a previously described mutation (Mcm5A7) that disrupts chromosome pairing, DSB repair is initiated by homologous recombination but is completed by non-homologous end joining (NHEJ). Remarkably, this process yields precise repair products. Our results provide support for a recombination intermediate recently proposed in mouse meiosis, in which an oligonucleotide bound to the Spo11 protein that catalyzes DSB formation remains bound after resection. We propose that this oligonucleotide functions as a primer for fill-in synthesis to allow scarless repair by NHEJ. We argue that this is a conserved repair mechanism that is likely to be invoked to overcome occasional challenges in normal meiosis.
机译：通过与同源染色体的重组来修复在减数分裂中的编程DNA双链断裂（DSB），以在所选地点产生往复式交叉，这对于在第一减数分裂划分中适当分离同源物的适当分离至关重要。备用修复过程可以在正常的减数分比重组过程非功能性时补偿。我们描述了一种新颖的备用修复机制，当在果蝇的果冻染色体中不可用时发生的备用修复机制。在破坏染色体配对的先前描述的突变（MCM5A7）的存在下，通过同源重组引发DSB修复，而是通过非同源末端接合（NHEJ）完成。值得注意的是，该过程产生精确的修复产品。我们的结果为最近提出的小鼠减数分裂中提出的重组中间体提供了支持，其中与催化DSB形成的SPO11蛋白结合的寡核苷酸保持在切除后仍然约束。我们提出这种寡核苷酸作为填充合成的底漆，以允许NHEJ无骨不干扰。我们认为这是一个可能被援引的保守维修机制，以克服普通减数分裂的偶尔挑战。

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