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Translesion DNA Synthesis

Overview
Journal EcoSal Plus
Specialty Microbiology
Date 2015 Oct 8
PMID 26442823
Citations 8
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Abstract

All living organisms are continually exposed to agents that damage their DNA, which threatens the integrity of their genome. As a consequence, cells are equipped with a plethora of DNA repair enzymes to remove the damaged DNA. Unfortunately, situations nevertheless arise where lesions persist, and these lesions block the progression of the cell's replicase. In these situations, cells are forced to choose between recombination-mediated "damage avoidance" pathways or a specialized DNA polymerase (pol) to traverse the blocking lesion. The latter process is referred to as Translesion DNA Synthesis (TLS). As inferred by its name, TLS not only results in bases being (mis)incorporated opposite DNA lesions but also bases being (mis)incorporated downstream of the replicase-blocking lesion, so as to ensure continued genome duplication and cell survival. Escherichia coli and Salmonella typhimurium possess five DNA polymerases, and while all have been shown to facilitate TLS under certain experimental conditions, it is clear that the LexA-regulated and damage-inducible pols II, IV, and V perform the vast majority of TLS under physiological conditions. Pol V can traverse a wide range of DNA lesions and performs the bulk of mutagenic TLS, whereas pol II and pol IV appear to be more specialized TLS polymerases.

Citing Articles

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Visualizing mutagenic repair: novel insights into bacterial translesion synthesis.

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References
1.
Neeley W, Delaney J, Henderson P, Essigmann J . In vivo bypass efficiencies and mutational signatures of the guanine oxidation products 2-aminoimidazolone and 5-guanidino-4-nitroimidazole. J Biol Chem. 2004; 279(42):43568-73. DOI: 10.1074/jbc.M407117200. View

2.
Patel M, Jiang Q, Woodgate R, Cox M, Goodman M . A new model for SOS-induced mutagenesis: how RecA protein activates DNA polymerase V. Crit Rev Biochem Mol Biol. 2010; 45(3):171-84. PMC: 2874081. DOI: 10.3109/10409238.2010.480968. View

3.
Bjedov I, Dasgupta C, Slade D, Le Blastier S, Selva M, Matic I . Involvement of Escherichia coli DNA polymerase IV in tolerance of cytotoxic alkylating DNA lesions in vivo. Genetics. 2007; 176(3):1431-40. PMC: 1931539. DOI: 10.1534/genetics.107.072405. View

4.
Boudsocq F, Kokoska R, Plosky B, Vaisman A, Ling H, Kunkel T . Investigating the role of the little finger domain of Y-family DNA polymerases in low fidelity synthesis and translesion replication. J Biol Chem. 2004; 279(31):32932-40. DOI: 10.1074/jbc.M405249200. View

5.
Indiani C, McInerney P, Georgescu R, Goodman M, ODonnell M . A sliding-clamp toolbelt binds high- and low-fidelity DNA polymerases simultaneously. Mol Cell. 2005; 19(6):805-15. DOI: 10.1016/j.molcel.2005.08.011. View