期刊
DNA REPAIR
卷 6, 期 11, 页码 1572-1583出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2007.05.004
关键词
DNA mismatch repair; EXO1; DNA nuclease; DNA damage and post-replication repair
资金
- NIGMS NIH HHS [R01 GM045413-15, R01 GM045413-13, R01 GM045413, R01 GM045413-16, GM45413, R01 GM045413-14] Funding Source: Medline
Replication forks stall at DNA lesions or as a result of an unfavorable replicative environment. These fork stalling events have been associated with recombination and gross chromosomal rearrangements. Recombination and fork bypass pathways are the mechanisms accountable for restart of stalled forks. An important lesion bypass mechanism is the highly conserved post-replication repair (PRR) pathway that is composed of error-prone translesion and error-free bypass branches. EXO1 codes for a Rad2p family member nuclease that has been implicated in a multitude of eukaryotic DNA metabolic pathways that include DNA repair, recombination, replication, and telomere integrity. In this report, we show EXO1 functions in the MMS2 error-free branch of the PRR pathway independent of the role of EXO1 in DNA mismatch repair (MMR). Consistent with the idea that EXO1 functions independently in two separate pathways, we defined a domain of Exo1p required for PRR distinct from those required for interaction with MMR proteins. We then generated a point mutant exo1 allele that was defective for the function of Exo1p in MMR due to disrupted interaction with Mlh1p, but still functional for PRR. Lastly, by using a compound exo1 mutant that was defective for interaction with Mlh1p and deficient for nuclease activity, we provide further evidence that Exo1p plays both structural and catalytic roles during MMR. (c) 2007 Elsevier B.V. All rights reserved.
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