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유전체항상성연구단
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MSH2-MSH3 promotes DNA end resection during homologous recombination and blocks polymerase theta-mediated end-joining through interaction with SMARCAD1 and EXO1

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Title
MSH2-MSH3 promotes DNA end resection during homologous recombination and blocks polymerase theta-mediated end-joining through interaction with SMARCAD1 and EXO1
Author(s)
Jung-Min Oh; Kang, Yujin; Park, Jumi; Yubin Sung; Kim, Dayoung; Yuri Seo; Eun A. Lee; Jae Sun Ra; Enkhzul Amarsanaa; Young-Un Park; Seon Young Lee; Jung Me Hwang; Hongtae Kim; Orlando Scharer; Seung Woo Cho; Lee, Changwook; Kei-ichi Takata; Ja Yil Lee; Kyungjae Myung
Publication Date
2023-06
Journal
NUCLEIC ACIDS RESEARCH, v.51, no.11, pp.5584 - 5602
Publisher
OXFORD UNIV PRESS
Abstract
DNA double-strand break (DSB) repair via homologous recombination is initiated by end resection. The extent of DNA end resection determines the choice of the DSB repair pathway. Nucleases for end resection have been extensively studied. However, it is still unclear how the potential DNA structures generated by the initial short resection by MRE11-RAD50-NBS1 are recognized and recruit proteins, such as EXO1, to DSB sites to facilitate long-range resection. We found that the MSH2-MSH3 mismatch repair complex is recruited to DSB sites through interaction with the chromatin remodeling protein SMARCAD1. MSH2-MSH3 facilitates the recruitment of EXO1 for long-range resection and enhances its enzymatic activity. MSH2-MSH3 also inhibits access of POL theta, which promotes polymerase theta-mediated end-joining (TMEJ). Collectively, we present a direct role of MSH2-MSH3 in the initial stages of DSB repair by promoting end resection and influencing the DSB repair pathway by favoring homologous recombination over TMEJ.
URI
https://pr.ibs.re.kr/handle/8788114/13633
DOI
10.1093/nar/gkad308
ISSN
0305-1048
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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