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Title: Chronological Switch from Translesion Synthesis to Homology-Dependent Gap Repair In Vivo

Abstract

Cells are constantly exposed to endogenous and exogenous chemical and physical agents that damage their genome by forming DNA lesions. These lesions interfere with the normal functions of DNA such as transcription and replication, and need to be either repaired or tolerated. DNA lesions are accurately removed via various repair pathways. In contrast, tolerance mechanisms do not remove lesions but only allow replication to proceed despite the presence of unrepaired lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS), which is an error-prone strategy and an accurate strategy based on homologous recombination (homology-dependent gap repair [HDGR]). Thus, the mutation frequency reflects the relative extent to which the two tolerance pathways operate in vivo. In the present paper, we review the present understanding of the mechanisms of TLS and HDGR and propose a novel and comprehensive view of the way both strategies interact and are regulated in vivo.

Authors:
 [1];  [1];  [1]
  1. DNA Damage Tolerance CNRS, Marseille (France); Institut Paoli-Calmettes, Marseille (France); Aix-Marseille Univ., Marseille (France); Inserm, Marseille (France)
Publication Date:
Research Org.:
Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
Sponsoring Org.:
USDOE Office of Science (SC)
OSTI Identifier:
1559160
Grant/Contract Number:  
AC02-05CH11231
Resource Type:
Accepted Manuscript
Journal Name:
Toxicological research
Additional Journal Information:
Journal Volume: 34; Journal Issue: 4; Journal ID: ISSN 1976-8257
Publisher:
Korean Society of Toxicology
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES

Citation Formats

Fujii, Shingo, Isogawa, Asako, and Fuchs, Robert P. Chronological Switch from Translesion Synthesis to Homology-Dependent Gap Repair In Vivo. United States: N. p., 2018. Web. doi:10.5487/TR.2018.34.4.297.
Fujii, Shingo, Isogawa, Asako, & Fuchs, Robert P. Chronological Switch from Translesion Synthesis to Homology-Dependent Gap Repair In Vivo. United States. doi:10.5487/TR.2018.34.4.297.
Fujii, Shingo, Isogawa, Asako, and Fuchs, Robert P. Mon . "Chronological Switch from Translesion Synthesis to Homology-Dependent Gap Repair In Vivo". United States. doi:10.5487/TR.2018.34.4.297. https://www.osti.gov/servlets/purl/1559160.
@article{osti_1559160,
title = {Chronological Switch from Translesion Synthesis to Homology-Dependent Gap Repair In Vivo},
author = {Fujii, Shingo and Isogawa, Asako and Fuchs, Robert P.},
abstractNote = {Cells are constantly exposed to endogenous and exogenous chemical and physical agents that damage their genome by forming DNA lesions. These lesions interfere with the normal functions of DNA such as transcription and replication, and need to be either repaired or tolerated. DNA lesions are accurately removed via various repair pathways. In contrast, tolerance mechanisms do not remove lesions but only allow replication to proceed despite the presence of unrepaired lesions. Cells possess two major tolerance strategies, namely translesion synthesis (TLS), which is an error-prone strategy and an accurate strategy based on homologous recombination (homology-dependent gap repair [HDGR]). Thus, the mutation frequency reflects the relative extent to which the two tolerance pathways operate in vivo. In the present paper, we review the present understanding of the mechanisms of TLS and HDGR and propose a novel and comprehensive view of the way both strategies interact and are regulated in vivo.},
doi = {10.5487/TR.2018.34.4.297},
journal = {Toxicological research},
number = 4,
volume = 34,
place = {United States},
year = {2018},
month = {10}
}

Journal Article:
Free Publicly Available Full Text
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