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UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides

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Title: UvrA and UvrB enhance mutations induced by oxidized deoxyribonucleotides
Authors: Hori, Mika Browse this author
Ishiguro, Chieko Browse this author
Suzuki, Tetsuya Browse this author
Nakagawa, Noriko Browse this author
Nunoshiba, Tatsuo Browse this author
Kuramitsu, Seiki Browse this author
Yamarnoto, Kazuo Browse this author
Kasai, Hiroshi Browse this author
Harashima, Hideyoshi Browse this author →KAKEN DB
Kamiya, Hiroyuki Browse this author
Keywords: UvrA
UvrB
8-hydroxy-dGTP
2-hydroxy-dATP
Issue Date: 1-Dec-2007
Publisher: Elsevier
Journal Title: DNA Repair
Volume: 6
Issue: 12
Start Page: 1786
End Page: 1793
Publisher DOI: 10.1016/j.dnarep.2007.06.013
PMID: 17709303
Abstract: Oxidatively damaged DNA precursors (deoxyribonucleotides) are formed by reactive oxygen species. After the damaged DNA precursors are incorporated into DNA, they might be removed by DNA repair enzymes. in this study, to examine whether a nucleotide excision repair enzyme, Escherichia coli UvrABC, could suppress the mutations induced by oxidized deoxyribonucleotides in vivo, oxidized DNA precursors, 8-hydroxy-2'-deoxyguanosine 5'-triphosphate and 2-hydroxy-2'-deoxyadenosine 5'-triphosphate, were introduced into uvrA, uvrB, and uvrC E. coli strains, and mutations in the chromosomal rpoB gene were analyzed. Unexpectedly, these oxidized DNA precursors induced mutations only slightly in the uvrA and uvrB strains. In contrast, effect of the uvrC-deficiency was not observed. Next, mutT, mutT/uvrA, and mutT/uvrB E. coli strains were treated with H_{2}O_{2}, and the rpoB mutant frequencies were calculated. The frequency of the H_{2}O_{2}-induced mutations was increased in all of the strains tested; however, the increase was three- to four-fold lower in the mutT/uvrA and mutT/uvrB strains than in the mutT strain. Thus, UvrA and UvrB are involved in the enhancement, but not in the suppression, of the mutations induced by these oxidized deoxyribonucleotides. These results suggest a novel role for UvrA and UvrB in the processing of oxidative damage.
Relation: http://www.sciencedirect.com/science/journal/15687864
Type: article (author version)
URI: http://hdl.handle.net/2115/32294
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 紙谷 浩之

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