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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
1988-2-20
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pubmed:abstractText |
Salmonella typhimurium strains containing deletions of oxyR, a positive regulator of defenses against oxidative stress, show 10- to 55-fold higher frequencies of spontaneous mutagenesis compared to otherwise isogenic oxyR+ control strains. The high spontaneous-mutation frequency in oxyR deletion strains is decreased by a factor of 3 when the strains are grown anaerobically. oxyR deletion strains show an increase in small deletion mutations and at least three of the six possible base-substitution mutations (T.A to A.T, C.G to T.A, and C.G to A.T). However, the largest increase in mutation frequency is observed for T.A to A.T transversions (40- to 146-fold), the base-substitution mutation most frequently caused by chemical oxidants. The introduction into oxyR deletion strains of multicopy plasmids carrying the oxyR-regulated genes for catalase (katG) or alkyl hydroperoxide reductase (ahp) results in overexpression of the respective enzyme activities and decreases the number of spontaneous mutants to wild-type levels. The introduction into oxyR deletions of a plasmid carrying the gene for superoxide dismutase (sodA) decreases the mutation frequency by a factor of 5 in some strain backgrounds. Strains that contain a dominant oxyR mutation and overexpress proteins regulated by oxyR show lower spontaneous-mutation frequencies by a factor of 2. These results indicate that oxyR and oxyR-regulated genes play a significant role in defense against spontaneous oxidative DNA damage. The role of oxidative damage to DNA in "spontaneous" mutagenesis is discussed.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-13278318,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-210504,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-2417830,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-2429316,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-2437576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-2988786,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-3022287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-3038676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-344891,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-3516975,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-3534881,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-3545059,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-368021,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-37532,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-3889622,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6094486,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6219285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6287922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6288657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6303219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6309739,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6341825,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6351251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6369329,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6371470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6379645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6383792,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6414957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6453349,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6592579,
http://linkedlifedata.com/resource/pubmed/commentcorrection/3321061-6760198
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
8917-21
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:3321061-Anaerobiosis,
pubmed-meshheading:3321061-Chromosome Deletion,
pubmed-meshheading:3321061-DNA, Bacterial,
pubmed-meshheading:3321061-DNA Damage,
pubmed-meshheading:3321061-Genes, Bacterial,
pubmed-meshheading:3321061-Genetic Complementation Test,
pubmed-meshheading:3321061-Mutation,
pubmed-meshheading:3321061-Oxidation-Reduction,
pubmed-meshheading:3321061-Oxygen,
pubmed-meshheading:3321061-Salmonella typhimurium
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pubmed:year |
1987
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pubmed:articleTitle |
Spontaneous mutagenesis and oxidative damage to DNA in Salmonella typhimurium.
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pubmed:affiliation |
Department of Biochemistry, University of California, Berkeley 94720.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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