tif-Stimulated deoxyribonucleic acid repair in Escherichia coli K-12

Castellazzi, Marc; Jacques, M; George, Jacqueline

doi:10.1128/jb.143.2.703-709.1980

Cited by 10 publications

(3 citation statements)

References 32 publications

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“…Our results demonstrate that the DNA damage-inducible SOS response plays a role in upregulating NER capacity in E. coli. The existence of such an upregulation after DNA damage has been previously postulated for several reasons, including (i) the demonstration that uvrA, uvrB, and uvrD were under Rec/Lex control and were induced rapidly after DNA damage (1,18,24,38); (ii) the dramatic increase in phage (5,48) and bacterial (5,12) survival if cells were preinduced by low flu- ences of UV or by genetic means; (iii) the reduced rate of CPD repair in recA mutants and the subsequent rapid rate of CPD repair when the SOS response was derepressed in the same cells (12); and (iv) the decrease in cell survival when protein synthesis treatments were given immediately following UV (13,39,40).…”

Section: Discussionmentioning

confidence: 99%

“…Studies of the relevance of SOS-dependent protein induction to NER have produced conflicting results. Castellazzi et al (5) showed that recA441 mutants, grown at 41°C to induce the SOS response, had an enhanced UV survival compared to an isogenic recA ϩ strain under the same conditions. The enhanced survival depended on de novo protein synthesis and the presence of wild-type uvrA.…”

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confidence: 99%

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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

Crowley

Hanawalt

1998

J Bacteriol

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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. InEscherichia 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.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Crowley

Hanawalt

1998

J Bacteriol

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“…It has also been reported that the lethal filamentation caused by low UV doses in an ruv-9 strain is not suppressed by the sfiAll mutation (20 (8). The sfiAll and sfiB103 mutations were further shown not to diminish tifor UV-induced reactivation of UV-inactivated A phage, and the sfiAll mutation does not affect tif-induced mutagenesis of A (5,8). Similarly, as shown in Fig.…”

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confidence: 93%

Further characterization of sfiA and sfiB mutations in Escherichia coli

Huisman¹,

D’Ari²,

George³

1980

J Bacteriol

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The sfiA and sfiB mutations, originally isolated in thermoresistant ultraviolet-resistant revertants of a tif lon strain, also suppressed filamentation in tsl strains (mutated at the lexA locus). When deoxyribonucleic acid synthesis was arrested, however, sfi-independent filamentation occurred. Other SOS functions were not affected by sfiA and sfiB mutations; in particular, ultraviolet-induced repair and mutagenesis of bacterial deoxyribonucleic acid were normal, as was tsl-tif-induced synthesis of recA protein. Genetic studies (i) established the identity of map location of the sfiA and sulA loci, (ii) showed that the two sfiB mutations are recessive, and (iii) showed that of six independent sfiA mutations, three are recessive and three are dominant. One sfiB strain was shown to have a 6% growth disadvantage relative to a sfi+ or sfiA strain. It is proposed that the sfiA locus may define the structural gene of a hypothetical inducible SOS-associated division inhibitor.

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Characterization of long patch excision repair of DNA in ultraviolet-irradiated Escherichia coli: An inducible function under rec-lex control

Cooper

1982

Molec. Gen. Genet.

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Excision repair in ultraviolet-irradiated wild-type Escherichia coli produces a bimodal distribution of repair patch sizes in the DNA. Approximately 99% of the repair events result in short patches of 20-30 nucleotides produced by a constitutive repair system. The remaining 1% result in patches which are at least 1,500 nucleotides in length. This long patch repair is shown to be a damage-inducible process under control of the rec-lex regulatory circuit. The kinetics of the two processes differ; short patch synthesis begins immediately after irradiation and is virtually completed prior to synthesis of the majority of the long patches. Long patch repair synthesis is a linear function of UV dose up to a plateau at 60 J/m2, and hence each long patch event is the consequence of a single UV-induced lesion. Long patch repair does not appear to be necessarily error-prone, since no alteration in repair synthesis occurs as a result of a mutation umuC- which renders cells nonmutable by UV. Evidence is presented suggesting that DNA polymerase I is responsible for both long and short patch synthesis in wild type cells under inducing conditions. In the absence of polymerase I the constitutive patch size averages 80-90 nucleotides, and this distribution is unchanged by induction.

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tif-Stimulated deoxyribonucleic acid repair in Escherichia coli K-12

Cited by 10 publications

References 32 publications

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

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

Further characterization of sfiA and sfiB mutations in Escherichia coli

Characterization of long patch excision repair of DNA in ultraviolet-irradiated Escherichia coli: An inducible function under rec-lex control

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