DNA mismatch repair and genetic instability

被引：486

作者：

Harfe, BD ^{[1
]}

Jinks-Robertson, S ^{[1
]}

机构：

[1] Emory Univ, Dept Biol, Atlanta, GA 30322 USA

来源：

ANNUAL REVIEW OF GENETICS | 2000年 / 34卷

关键词：

mutation; mutator; recombination; DNA damage; cancer;

D O I：

10.1146/annurev.genet.34.1.359

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Mismatch repair (MMR) systems play a central role in promoting genetic stability by repairing DNA replication errors, inhibiting recombination between non-identical DNA sequences and participating in responses to DNA damage. The discovery of a link between human cancer and MMR defects has led to an explosion of research on eukaryotic MMR. The key proteins in MMR are highly conserved from bacteria to mammals, and this conservation has been critical for defining the components of eukaryotic MMR systems. In eukaryotes, there are multiple homologs of the key bacterial MutS and MutL MMR proteins, and these homologs form heterodimers that have discrete roles in MMR-related processes. This review describes the genetic and biochemical approaches used to study MMR, and summarizes the diverse roles that MMR proteins play in maintaining genetic stability.

引用

页码：359 / 399

页数：43

共 239 条

[41] Arabidopsis MutS homologs-AtMSH2, AtMSH3, AtMSH6, and a novel AtMSH7-form three distinct protein heterodimers with different specificities for mismatched DNA [J].