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首页> 外文期刊>Molecular and Cellular Biology >Evidence for Biased Holliday Junction Cleavage and Mismatch Repair Directed by Junction Cuts during Double-Strand-Break Repair in Mammalian Cells
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Evidence for Biased Holliday Junction Cleavage and Mismatch Repair Directed by Junction Cuts during Double-Strand-Break Repair in Mammalian Cells

机译：哺乳动物细胞双链断裂修复过程中霍奇迪交界处的裂解和错配修复的证据。

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In mammalian cells, several features of the way homologous recombination occurs between transferred and chromosomal DNA are consistent with the double-strand-break repair (DSBR) model of recombination. In this study, we examined the segregation patterns of small palindrome markers, which frequently escape mismatch repair when encompassed within heteroduplex DNA formed in vivo during mammalian homologous recombination, to test predictions of the DSBR model, in particular as they relate to the mechanism of crossover resolution. According to the canonical DSBR model, crossover between the vector and chromosome results from cleavage of the joint molecule in two alternate sense modes. The two crossover modes lead to different predicted marker configurations in the recombinants, and assuming no bias in the mode of Holliday junction cleavage, the two types of recombinants are expected in equal frequency. However, we propose a revision to the canonical model, as our results suggest that the mode of crossover resolution is biased in favor of cutting the DNA strands upon which DNA synthesis is occurring during formation of the joint molecule. The bias in junction resolution permitted us to examine the potential consequences of mismatch repair acting on the DNA breaks generated by junction cutting. The combination of biased junction resolution with both early and late rounds of mismatch repair can explain the marker patterns in the recombinants.
机译：在哺乳动物细胞中，转移的和染色体的DNA之间发生同源重组的方式的一些特征与重组的双链断裂修复（DSBR）模型一致。在这项研究中，我们检查了小的回文标记的分离模式，当其被包含在哺乳动物同源重组过程中体内形成的异源双链DNA中时，常常会逃脱错配修复，以测试DSBR模型的预测，特别是因为它们与交叉机制有关解析度。根据规范的DSBR模型，载体和染色体之间的交换是由两种交替的有义模式下的联合分子裂解所致。两种交换模式导致重组体中不同的预测标记构型，并且假设在霍利迪连接裂解的模式中没有偏差，则预期两种类型的重组体的频率相同。但是，我们建议对规范模型进行修订，因为我们的结果表明交叉分辨率的模式偏向于有利于切割在形成联合分子期间发生DNA合成的DNA链。连接分辨率的偏差使我们能够研究错配修复对连接切割产生的DNA断裂的潜在作用。偏向接头分辨率与错配修复的早期和晚期回合的结合可以解释重组体中的标记模式。

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