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유전체 항상성 연구단
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ATAD5 promotes replication restart by regulating RAD51 and PCNA in response to replication stress

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Title
ATAD5 promotes replication restart by regulating RAD51 and PCNA in response to replication stress
Author(s)
Su Hyung Park; Nalae Kang; Song E.; Wie M.; Eun A. Lee; Sunyoung Hwang; Lee D.; Jae Sun Ra; In Bae Park; Jieun Park; Sukhyun Kang; Jun Hong Park; Hohng S.; Kyoo-young Lee; Kyungjae Myung
Publication Date
2019-12
Journal
NATURE COMMUNICATIONS, v.10, no.1, pp.5718 -
Publisher
NATURE PUBLISHING GROUP
Abstract
© 2019, The Author(s).Maintaining stability of replication forks is important for genomic integrity. However, it is not clear how replisome proteins contribute to fork stability under replication stress. Here, we report that ATAD5, a PCNA unloader, plays multiple functions at stalled forks including promoting its restart. ATAD5 depletion increases genomic instability upon hydroxyurea treatment in cultured cells and mice. ATAD5 recruits RAD51 to stalled forks in an ATR kinase-dependent manner by hydroxyurea-enhanced protein-protein interactions and timely removes PCNA from stalled forks for RAD51 recruitment. Consistent with the role of RAD51 in fork regression, ATAD5 depletion inhibits slowdown of fork progression and native 5-bromo-2ʹ-deoxyuridine signal induced by hydroxyurea. Single-molecule FRET showed that PCNA itself acts as a mechanical barrier to fork regression. Consequently, DNA breaks required for fork restart are reduced by ATAD5 depletion. Collectively, our results suggest an important role of ATAD5 in maintaining genome integrity during replication stress
URI
https://pr.ibs.re.kr/handle/8788114/6720
ISSN
2041-1723
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > Journal Papers (저널논문)
Files in This Item:
Nat. Comm._2019_ATAD5 promotes replication restart by regulating RAD51 and PCNA in response to replication stress.pdfDownload

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