Document Type

Post-Print

Publication Date

8-2016

Subjects

DNA repair, Genetic recombination

Abstract

DNA interstrand crosslinks are complex lesions that covalently link both strands of the duplex DNA. Lesion removal is proposed to initiate via the UvrABC nucleotide excision repair complex, however less is known about the subsequent steps of this complex repair pathway. In this study, we characterized the contribution of nucleotide excision repair mutants to survival in the presence of psoralen-induced damage. Unexpectedly, we observed that the nucleotide excision repair mutants exhibit differential sensitivity to psoralen-induced damage, with uvrC mutants being less sensitive than either uvrA or uvrB. We show that Cho, an alternative endonuclease, acts with UvrAB and is responsible for the reduced hypersensitivity of uvrC mutants. We find that Cho's contribution to survival correlates with the presence of DNA interstrand crosslinks, rather than monoadducts, and operates at a step after, or independent from, the initial incision during the global repair of psoralen DNA adducts from the genome.

Description

NOTICE: this is the author’s version of a work that was accepted for publication in Journal of Bacteriology. Changes resulting from the publishing process. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published at: https://doi.org/10.1128/JB.00509-16

DOI

10.1128/JB.00509-16

Persistent Identifier

http://archives.pdx.edu/ds/psu/18435

Included in

Biology Commons

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