Sequential assembly of translesion DNA polymerases at UV-induced DNA damage sites

Andersen, Parker L.; Xu, Fang; Ziola, Barry; McGregor, W. Glen; Xiao, Wei

doi:10.1091/mbc.e10-12-0938

Cited by 33 publications

(36 citation statements)

References 60 publications

(99 reference statements)

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“…REV1 probably has a PCNA-binding site(s) in its C-terminal region (12,46,47). Furthermore, although Akagi et al (48) have shown that the accumulation of human endogenous REV1 into locally UV-irradiated regions of nucleus depends on the interaction with pol , Andersen et al (45) have reported that the recruitment of the human endogenous REV1 is independent of the interaction with pol . Our results obtained in TKO, DKO, and Rad18…”

Section: Discussionmentioning

confidence: 99%

The Vital Role of Polymerase ζ and REV1 in Mutagenic, but Not Correct, DNA Synthesis across Benzo[a]pyrene-dG and Recruitment of Polymerase ζ by REV1 to Replication-stalled Site

Hashimoto

Cho

Yang

et al. 2012

Journal of Biological Chemistry

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Background: dG lesion derived from potent carcinogen benzo[a]pyrene causes mutations through DNA replication. Results: Pol and REV1 are essential to mutagenic, but not accurate, translesion DNA synthesis. Conclusion: DNA synthesis across identical DNA damage can be catalyzed by a different set of polymerases. Significance: The results have revealed an important role for DNA polymerases, pol and REV1, in inducing mutations.

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Section: Discussionmentioning

confidence: 99%

The Vital Role of Polymerase ζ and REV1 in Mutagenic, but Not Correct, DNA Synthesis across Benzo[a]pyrene-dG and Recruitment of Polymerase ζ by REV1 to Replication-stalled Site

Hashimoto

Cho

Yang

et al. 2012

Journal of Biological Chemistry

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“…of Pages 9 UV light these translesion synthesis polymerases accumulate at nuclear foci, which may represent sites of stalled replication forks. The formation of Pol foci strongly relies on Rev1 [81], which most likely recruits Pol to UV-induced (6-4)PPs and subsequently prevents nucleotide slippage by Pol during DNA synthesis [82]. Whether the nuclear localization of mammalian Rev1 to UV-induced nucleotide lesions requires Pol is still a matter of debate [53,81,83].…”

Section: Recruitment Of Translesion Synthesis Polymerases To Stalled mentioning

confidence: 99%

Roles of mutagenic translesion synthesis in mammalian genome stability, health and disease

2015

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“…Introduction of the bulky lesions consisting of CPDs and 6-4PPs blocks replicative polymerases and triggers the DDT pathway in which TLS polymerases switch places with the replicative polymerases and bypass the lesions [Andersen et al, 2011]. The key event that initiates TLS is the monoubiquitination of PCNA by RAD18/RAD6 [Hoege et al, 2002;Lehmann, 2011].…”

Section: Roles Of Pol D3 In Translesion Synthesis By Tls Polymerasesçmentioning

confidence: 99%

Regulation of human DNA polymerase delta in the cellular responses to DNA damage

Lee

Zhang

Lin

et al. 2012

Environ and Mol Mutagen

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The p12 subunit of polymerase delta (Pol d) is degraded in response to DNA damage induced by UV, alkylating agents, oxidative, and replication stresses. This leads to the conversion of the Pol d4 holoenzyme to the heterotrimer, Pol d3. We review studies that establish that Pol d3 formation is an event that could have a major impact on cellular processes in genomic surveillance, DNA replication, and DNA repair. p12 degradation is dependent on the apical ataxia telangiectasia and Rad3 related (ATR) kinase and is mediated by the ubiquitin-proteasome system. Pol d3 exhibits properties of an ''antimutator'' polymerase, suggesting that it could contribute to an increased surveillance against mutagenesis, for example, when Pol d carries out bypass synthesis past small base lesions that engage in spurious base pairing. Chromatin immunoprecipitation analysis and examination of the spatiotemporal recruitment of Pol d to sites of DNA damage show that Pol d3 is the primary form of Pol d associated with cyclobutane pyrimidine dimer lesions and therefore should be considered as the operative form of Pol d engaged in DNA repair. We propose a model for the switching of Pol d with translesion polymerases, incorporating the salient features of the recently determined structure of monoubiquitinated proliferating cell nuclear antigen and emphasizing the role of Pol d3. Because of the critical role of Pol d activity in DNA replication and repair, the formation of Pol d3 in response to DNA damage opens the prospect that pleiotropic effects may ensue. This opens the horizons for future exploration of how this novel response to DNA damage contributes to genomic stability. Environ. Mol. Mutagen. 53:683-698, 2012. V V C 2012 Wiley Periodicals, Inc.

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Sequential assembly of translesion DNA polymerases at UV-induced DNA damage sites

Abstract: Three endogenous translesion DNA polymerases are sequentially assembled to the stalled replication site in the form of UV-induced nuclear foci. Detailed supporting evidence is given for the polymerase switch model.

Cited by 33 publications

References 60 publications

The Vital Role of Polymerase ζ and REV1 in Mutagenic, but Not Correct, DNA Synthesis across Benzo[a]pyrene-dG and Recruitment of Polymerase ζ by REV1 to Replication-stalled Site

The Vital Role of Polymerase ζ and REV1 in Mutagenic, but Not Correct, DNA Synthesis across Benzo[a]pyrene-dG and Recruitment of Polymerase ζ by REV1 to Replication-stalled Site

Roles of mutagenic translesion synthesis in mammalian genome stability, health and disease

Regulation of human DNA polymerase delta in the cellular responses to DNA damage

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