Exonuclease 1-dependent and independent mismatch repair

被引:106
作者
Goellner, Eva M. [1 ]
Putnam, Christopher D. [1 ,2 ]
Kolodner, Richard D. [1 ,3 ,4 ,5 ,6 ]
机构
[1] Ludwig Inst Canc Res, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, San Diego Sch Med, Dept Med, La Jolla, CA 92093 USA
[3] Univ Calif San Diego, San Diego Sch Med, Dept Cellular, La Jolla, CA 92093 USA
[4] Univ Calif San Diego, San Diego Sch Med, Dept Mol Med, La Jolla, CA 92093 USA
[5] Univ Calif San Diego, San Diego Sch Med, Moores UCSD Canc Ctr, La Jolla, CA 92093 USA
[6] Univ Calif San Diego, San Diego Sch Med, Inst Genom Med, La Jolla, CA 92093 USA
关键词
Msh2-Msh6; Mlh1-Pms1; Mutagenesis; DNA replication fidelity; Mispaired base; Excision; Recombination; CELL NUCLEAR ANTIGEN; SACCHAROMYCES-CEREVISIAE MSH2-MSH6; NUCLEOTIDE EXCISION-REPAIR; ESCHERICHIA-COLI MUTS; DNA-MISMATCH; MISPAIR-RECOGNITION; CHECKPOINT ACTIVATION; MUTATION AVOIDANCE; COLORECTAL-CANCER; CRYSTAL-STRUCTURE;
D O I
10.1016/j.dnarep.2015.04.010
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
DNA mismatch repair (MMR) acts to repair mispaired bases resulting from misincorporation errors during DNA replication and also recognizes mispaired bases in recombination (HR) intermediates. Exonuclease I (Exo1) is a 5 ' -> 3 ' exonuclease that participates in a number of DNA repair pathways. Exo1 was identified as an exonuclease that participates in Saccharomyces cerevisiae and human MMR where it functions to excise the daughter strand after mispair recognition, and additionally Exo1 functions in end resection during HR. However, Exo1 is not absolutely required for end resection during HR in vivo. Similarly, while Exo1 is required in MMR reactions that have been reconstituted in vitro, genetics studies have shown that it is not absolutely required for MMR in vivo suggesting the existence of Exo1-independent and Exo1 -dependent MMR subpathways. Here, we review what is known about the Exo1 -independent and Exo1-dependent subpathways, including studies of mutations in MMR genes that specifically disrupt either subpathway. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:24 / 32
页数:9
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