The Saccharomyces cerevisiae Msh2 mismatch repair protein localizes to recombination intermediates in vivo
The Saccharomyces cerevisiae Msh2 mismatch repair protein localizes to recombination intermediates in vivo
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DOI：
10.1016/s1097-2765(00)80319-6
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发表时间：
2000-05-01
期刊：
影响因子：
16
通讯作者：
Alani, E
中科院分区：
文献类型：
--
作者：
Evans, E;Sugawara, N;Alani, E
错配修复蛋白在双链断裂修复（DSBR）过程中起作用，以纠正异源双链DNA中的错配，抑制不同序列之间的重组，并促进去除DSB末端的非同源DNA。我们研究了酵母Msh 2 p协会与重组中间体在体内使用染色质免疫沉淀。在涉及非同源末端的DSBR期间，Msh 2 p强烈定位于受体和供体序列。定位需要Msh 3 p，并且在rad 50 Delta菌株中大大减少。在完全同源修复过程中观察到Msh 2 p的最小定位，但这在rad 52 Delta菌株中增加。这些发现表明，Msh 2 p-Msh 3 p与DSBR早期的中间体相关，参与了同源配对的排斥，并稳定了Rad 1 p-Rad 10 p核酸内切酶切割的非同源尾。
Mismatch repair proteins act during double-strand break repair (DSBR) to correct mismatches in heteroduplex DNA, to suppress recombination between divergent sequences, and to promote removal of nonhomologous DNA at DSB ends. We investigated yeast Msh2p association with recombination intermediates in vivo using chromatin immunoprecipitation. During DSBR involving nonhomologous ends, Msh2p localized strongly to recipient and donor sequences. Localization required Msh3p and was greatly reduced in rad50 Delta strains. Minimal localization of Msh2p was observed during fully homologous repair, but this was increased in rad52 Delta strains. These findings argue that Msh2p-Msh3p associates with intermediates early in DSBR to participate in the rejection of homeologous pairing and to stabilize nonhomologous tails for cleavage by Rad1p-Rad10p endonuclease.