Roles for mismatch repair family proteins in promoting meiotic crossing over.
Roles for mismatch repair family proteins in promoting meiotic crossing over.
复制标题
DOI：
10.1016/j.dnarep.2015.11.024
复制
发表时间：
2016-02
期刊：
影响因子：
3.8
通讯作者：
Alani E
中科院分区：
文献类型：
--
作者：
Manhart CM;Alani E
错配修复（MMR）家族复合体Msh4-Msh5和Mlh1-Mlh3在减数分裂双链断裂修复途径中与Exo1和Sgs1-Top3-Rmi1作用，导致双Holliday结（dHJ）的不对称切割形成交叉。这篇综述讨论了Msh4-Msh5和Mlh1-Mlh3在减数分裂中的作用如何不符合复制后MMR的模式。我们还概述了用于解释这些因素如何促进减数分裂交叉形成的模型，这些交叉是在减数分裂I分裂期间染色体同源物精确分离所必需的。
The mismatch repair (MMR) family complexes Msh4-Msh5 and Mlh1-Mlh3 act with Exo1 and Sgs1-Top3-Rmi1 in a meiotic double strand break repair pathway that results in the asymmetric cleavage of double Holliday junctions (dHJ) to form crossovers. This review discusses how meiotic roles for Msh4-Msh5 and Mlh1-Mlh3 do not fit paradigms established for post-replicative MMR. We also outline models used to explain how these factors promote the formation of meiotic crossovers required for the accurate segregation of chromosome homologs during the Meiosis I division.