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Control of DNA Damage Bypass by Ubiquitylation of PCNA

Department of Biochemistry, University of Iowa College of Medicine, Iowa City, IA 52242-1109, USA
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Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Genes 2020, 11(2), 138; https://doi.org/10.3390/genes11020138
Received: 14 January 2020 / Revised: 23 January 2020 / Accepted: 27 January 2020 / Published: 29 January 2020
(This article belongs to the Special Issue Protective Mechanisms Against DNA Replication Stress)
DNA damage leads to genome instability by interfering with DNA replication. Cells possess several damage bypass pathways that mitigate the effects of DNA damage during replication. These pathways include translesion synthesis and template switching. These pathways are regulated largely through post-translational modifications of proliferating cell nuclear antigen (PCNA), an essential replication accessory factor. Mono-ubiquitylation of PCNA promotes translesion synthesis, and K63-linked poly-ubiquitylation promotes template switching. This article will discuss the mechanisms of how these post-translational modifications of PCNA control these bypass pathways from a structural and biochemical perspective. We will focus on the structure and function of the E3 ubiquitin ligases Rad18 and Rad5 that facilitate the mono-ubiquitylation and poly-ubiquitylation of PCNA, respectively. We conclude by reviewing alternative ideas about how these post-translational modifications of PCNA regulate the assembly of the multi-protein complexes that promote damage bypass pathways.
Keywords: DNA repair; DNA replication; Rad5; Rad18; translesion synthesis; template switching DNA repair; DNA replication; Rad5; Rad18; translesion synthesis; template switching
MDPI and ACS Style

Ripley, B.M.; Gildenberg, M.S.; Washington, M.T. Control of DNA Damage Bypass by Ubiquitylation of PCNA. Genes 2020, 11, 138.

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