Publication: Transcriptional Repressor ZBTB1 Promotes Chromatin Remodeling and Translesion DNA Synthesis
Issued Date
2014-04-10
Resource Type
ISSN
10974164
10972765
10972765
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2-s2.0-84898043561
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Mahidol University
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SCOPUS
Bibliographic Citation
Molecular Cell. Vol.54, No.1 (2014), 107-118
Suggested Citation
Hyungjin Kim, Donniphat Dejsuphong, Guillaume Adelmant, Raphael Ceccaldi, Kailin Yang, Jarrod A. Marto, Alan D. D'Andrea Transcriptional Repressor ZBTB1 Promotes Chromatin Remodeling and Translesion DNA Synthesis. Molecular Cell. Vol.54, No.1 (2014), 107-118. doi:10.1016/j.molcel.2014.02.017 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/33278
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Title
Transcriptional Repressor ZBTB1 Promotes Chromatin Remodeling and Translesion DNA Synthesis
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Abstract
Timely DNA replication across damaged DNA is critical for maintaining genomic integrity. Translesion DNA synthesis (TLS) allows bypass of DNA lesions using error-prone TLS polymerases. The E3 ligase RAD18 is necessary for proliferating cell nuclear antigen (PCNA) monoubiquitination and TLS polymerase recruitment; however, the regulatory steps upstream of RAD18 activation are less understood. Here, we show that the UBZ4 domain-containing transcriptional repressor ZBTB1 is a critical upstream regulator of TLS. The UBZ4 motif is required for PCNA monoubiquitination and survival after UV damage. ZBTB1 associates with KAP-1, a transcriptional repressor whose phosphorylation relaxes chromatin after DNA damage. ZBTB1 depletion impairs formation of phospho-KAP-1 at UV damage sites and reduces RAD18 recruitment. Furthermore, phosphorylation of KAP-1 is necessary for efficient PCNA modification. We propose that ZBTB1 is required for localizing phospho-KAP-1 to chromatin and enhancing RAD18 accessibility. Collectively, our study implicates a ubiquitin-binding protein in orchestrating chromatin remodeling during DNA repair. © 2014 Elsevier Inc.