Two pathways for removal of nonhomologous DNA ends during double-strand break repair in Saccharomyces cerevisiae

Two pathways for removal of nonhomologous DNA ends during double-strand break repair in Saccharomyces cerevisiae
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DOI:
10.1128/mcb.17.11.6765
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发表时间:
1997-11-01
影响因子:
5.3
通讯作者:
Haber, JE
Haber, JE
中科院分区:
生物学2区
文献类型:
--
作者:
Paques, F;Haber, JE

文献摘要

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在通过基因转换修复双链断裂(DSB)期间,DSB的一个或两个3'端侵入同源供体序列并启动新的DNA合成。使用入侵DNA链作为新DNA合成的引物需要去除3'端的任何非同源碱基。我们先前已经表明,在酿酒酵母中去除3'非同源尾依赖于核苷酸切除修复核酸内切酶Rad 1/Rad 10,并且还依赖于错配修复蛋白Msh 2和Msh 3,我们现在报告说,这四个蛋白质只需要当重组DNA的非同源末端是30个核苷酸(nt)长或更长。另外一种蛋白质,解旋酶Srs 2,需要RAD 1依赖性去除长的3'尾巴。我们认为Srs 2的作用是延长和稳定入侵单链及其同源物之间的初始新生连接,3'尾短于30 nt的被删除的另一种机制,至少部分取决于3'到5'校对活动的DNA聚合酶δ。
During repair of a double-strand break (DSB) by gene conversion, one or both 3' ends of the DSB invade a homologous donor sequence and initiate new DNA synthesis. The use of the invading DNA strand as a primer for new DNA synthesis requires that any nonhomologous bases at the 3' end be removed, We have previously shown that removal of a 3' nonhomologous tail in Saccharomyces cerevisiae depends on the nucleotide excision repair endonuclease Rad1/Rad10, and also on the mismatch repair proteins Msh2 and Msh3, We now report that these four proteins are needed only when the nonhomologous ends of recombining DNA are 30 nucleotides (nt) long or longer. An additional protein, the helicase Srs2, is required for the RAD1-dependent removal of long 3' tails. We suggest that Srs2 acts to extend and stabilize the initial nascent joint between the invading single strand and its homolog, 3' tails shorter than 30 nt are removed by another mechanism that depends at least in part on the 3'-to-5' proofreading activity of DNA polymerase delta.