Evans E, Sugawara N, Haber J E, Alani E
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA.
Mol Cell. 2000 May;5(5):789-99. doi: 10.1016/s1097-2765(00)80319-6.
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 rad50delta strains. Minimal localization of Msh2p was observed during fully homologous repair, but this was increased in rad52delta 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.
错配修复蛋白在双链断裂修复（DSBR）过程中发挥作用，以纠正异源双链DNA中的错配，抑制不同序列之间的重组，并促进双链断裂末端非同源DNA的去除。我们使用染色质免疫沉淀技术在体内研究了酵母Msh2p与重组中间体的关联。在涉及非同源末端的DSBR过程中，Msh2p强烈定位于受体和供体序列。这种定位需要Msh3p，并且在rad50delta菌株中大大减少。在完全同源修复过程中观察到Msh2p的定位极少，但在rad52delta菌株中这种定位增加。这些发现表明，Msh2p-Msh3p在DSBR早期与中间体结合，参与同源配对的排斥，并稳定非同源尾巴以便被Rad1p-Rad10p核酸内切酶切割。
