Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1998-7-27
pubmed:abstractText
Nucleotide excision repair (NER) is responsible for the removal of a variety of lesions from damaged DNA and proceeds through two subpathways, global repair and transcription-coupled repair. In Escherichia coli, both subpathways require UvrA and UvrB, which are induced following DNA damage as part of the SOS response. We found that elimination of the SOS response either genetically or by treatment with the transcription inhibitor rifampin reduced the efficiency of global repair of the major UV-induced lesion, the cyclobutane pyrimidine dimer (CPD), but had no effect on the global repair of 6-4 photoproducts. Mutants in which the SOS response was constitutively derepressed repaired CPDs more rapidly than did wild-type cells, and this rate was not affected by rifampin. Transcription-coupled repair of CPDs occurred in the absence of SOS induction but was undetectable when the response was expressed constitutively. These results suggest that damage-inducible synthesis of UvrA and UvrB is necessary for efficient repair of CPDs and that the levels of these proteins determine the rate of NER of UV photoproducts. We compare our findings with recent data from eukaryotic systems and suggest that damage-inducible stress responses are generally critical for efficient global repair of certain types of genomic damage.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-14265747, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-1549511, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-16589315, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-1763073, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-1780359, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-2554145, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-2670681, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-2672059, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-3050123, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-319458, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-3217441, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-329100, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-366385, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-3664636, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-3838150, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-3911024, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-4559738, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-4923859, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-4990763, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6208364, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6298183, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6319240, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6371470, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6451614, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6771759, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6780917, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-6802798, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-7045579, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-7526203, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-7568035, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8349576, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8423816, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8465200, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8486719, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8510656, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8577757, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8631712, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-87138, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-8811174, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-9304113, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-9346961, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-9356435, http://linkedlifedata.com/resource/pubmed/commentcorrection/9642186-9356500
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9193
pubmed:author
pubmed:issnType
Print
pubmed:volume
180
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3345-52
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Induction of the SOS response increases the efficiency of global nucleotide excision repair of cyclobutane pyrimidine dimers, but not 6-4 photoproducts, in UV-irradiated Escherichia coli.
pubmed:affiliation
Department of Biological Sciences, Stanford University, California 94305-5020, USA. dcrowley@leland.stanford.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.