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Genes 2017, 8(2), 64; doi:10.3390/genes8020064

Mechanisms of Post-Replication DNA Repair

1
Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA
2
Curriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599,USA
*
Author to whom correspondence should be addressed.
Received: 5 December 2016 / Accepted: 3 February 2017 / Published: 8 February 2017
(This article belongs to the Special Issue DNA Replication Controls)
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Abstract

Accurate DNA replication is crucial for cell survival and the maintenance of genome stability. Cells have developed mechanisms to cope with the frequent genotoxic injuries that arise from both endogenous and environmental sources. Lesions encountered during DNA replication are often tolerated by post-replication repair mechanisms that prevent replication fork collapse and avert the formation of DNA double strand breaks. There are two predominant post-replication repair pathways, trans-lesion synthesis (TLS) and template switching (TS). TLS is a DNA damage-tolerant and low-fidelity mode of DNA synthesis that utilizes specialized ‘Y-family’ DNA polymerases to replicate damaged templates. TS, however, is an error-free ‘DNA damage avoidance’ mode of DNA synthesis that uses a newly synthesized sister chromatid as a template in lieu of the damaged parent strand. Both TLS and TS pathways are tightly controlled signaling cascades that integrate DNA synthesis with the overall DNA damage response and are thus crucial for genome stability. This review will cover the current knowledge of the primary mediators of post-replication repair and how they are regulated in the cell. View Full-Text
Keywords: DNA damage tolerance; post replication repair; DNA damage response; trans-lesion synthesis; template switching DNA damage tolerance; post replication repair; DNA damage response; trans-lesion synthesis; template switching
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Gao, Y.; Mutter-Rottmayer, E.; Zlatanou, A.; Vaziri, C.; Yang, Y. Mechanisms of Post-Replication DNA Repair. Genes 2017, 8, 64.

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