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Myung, Kyungjae
Center for Genomic Integrity
Research Interests
  • DNA Replication, DNA Repair, DNA Recombination, DNA Damage Response, cancer, aging

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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
Park, Su HyungKang, NalaeSong, EunhoWie, MinwooLee, Eun A.Hwang, SunyoungLee, DeokjaeRa, Jae SunPark, In BaePark, JieunKang, SukhyunPark, Jun HongHohng, SungchulLee, Kyoo-youngMyung, Kyungjae
Issue Date
2019-12
Publisher
Nature Publishing Group
Citation
NATURE COMMUNICATIONS, v.10, no.1, pp.5718
Abstract
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://scholarworks.unist.ac.kr/handle/201301/30643
URL
https://www.nature.com/articles/s41467-019-13667-4
DOI
10.1038/s41467-019-13667-4
ISSN
2041-1723
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SLS_Journal Papers
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