CST复合物介导切除后非同源末端连接修复途径,并促进酿酒酵母的局部缺失。

IF 11.1 Q1 CELL BIOLOGY
Oana Ilioaia, Liébaut Dudragne, Clémentine Brocas, Léa Meneu, Romain Koszul, Karine Dubrana, Zhou Xu
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引用次数: 0

摘要

通过非同源末端连接(NHEJ)修复DNA双链断裂(DSB)通常会留下一个完整或最小修饰的序列。切除暴露单链DNA,并将修复导向同源依赖途径,远离NHEJ。在这里,我们报道了在酿酒酵母中,Cdc13/Stn1/Ten1 (CST)复合物,以其端粒功能为特征,在切除起始后介导备用NHEJ修复。我们发现修复后的cst特异性突变特征为5-85 bp的缺失,主要依赖于NHEJ,其中一小部分依赖于微同源介导的末端连接(MMEJ)。CST和pol α-引物酶之间的相互作用对于这些中等大小的缺失是至关重要的,这表明CST和pol α-引物酶之间存在填补合成的作用,从而限制了广泛的切除,否则会导致数千个碱基的mmej依赖性缺失。总的来说,这些结果描绘了修复途径选择的复杂图景,其中CST促进了切除后NHEJ的修复,促进了局部缺失,但防止了更大的和潜在更有害的缺失和重排。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The CST complex mediates a post-resection non-homologous end joining repair pathway and promotes local deletions in Saccharomyces cerevisiae.

The repair of a DNA double-strand break (DSB) by non-homologous end joining (NHEJ) generally leaves an intact or minimally modified sequence. Resection exposes single-stranded DNA and directs repair toward homology-dependent pathways and away from NHEJ. Here, we report that in Saccharomyces cerevisiae, the Cdc13/Stn1/Ten1 (CST) complex, characterized for its telomeric functions, acts after resection initiation to mediate a back-up NHEJ repair. We found a CST-specific mutation signature after repair characterized by deletions of 5-85 bp that were mostly dependent on NHEJ, with a subset dependent on microhomology-mediated end joining (MMEJ). The interaction between CST and Polα-primase is critical for these intermediate-size deletions, suggesting a role for fill-in synthesis, thus limiting extensive resection, which would otherwise lead to MMEJ-dependent deletions of several kilobases. Collectively, these results depict a complex picture of repair pathway choice where CST facilitates post-resection NHEJ repair, promoting local deletions but guarding against larger and potentially more deleterious deletions and rearrangements.

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CiteScore
7.10
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