UV-inducible repair II: Its role in various defective mutants of Escherichia coli K-12

Sedliaková, Milena; Slezáriková, V.; Piršel, Miroslav

doi:10.1007/bf00266914

Cited by 15 publications

(4 citation statements)

References 26 publications

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“…Further characterization indicated that the lac fusion was indeed to the uvrA gene, and thus that at least one of the SOS-regulated loci identified by this procedure actually coded for a gene product (172). The observation that the uvrA gene was inducible was consistent with a series of in vivo observations indicating that uvr+-dependent repair processes can be induced in E. coli (57,58,319,320).…”

Section: Downloaded Fromsupporting

confidence: 77%

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

Walker¹

1984

Microbiological Reviews

1,035

410

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Section: Downloaded Fromsupporting

confidence: 77%

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

Walker¹

1984

Microbiological Reviews

1,035

410

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“…The process in question is a complex one. Previous data (Sedliakova' et al, 1978b) appear to indicate that it requires at least four genes to function, namely, uvrA, uvrB, lexA and recA.…”

Section: Discussionmentioning

confidence: 93%

Evidence that dimers remaining in preinduced Escherichia coli B/r Hcr+ become insensitive after DNA replication to the extract from Micrococcus luteus

Sedliaková¹,

Brozmanová²,

Mašek³

et al. 1981

Biophysical Journal

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In Escherichia coli B/r Her+ irradiated with two separate fluences, dimer excision is prematurely interrupted. The present study was designed to follow tha fate of dimers remaining unexcised. The results imply that these dimers (or distortions containing dimers) are transformed on replication from the state of sensitivity to the state of insensitivity to endonuclease from Micrococcus luteus. This conclusion is based on the following findings: (a) dimers were radiochromatographically detectable in DNA replicated after UV, which indicated that they were tolerated on replication. (b) Similar amounts of dimers were detected radiochromatographically both in DNA remaining unreplicated and DNA twice replicated after UV, This along with the low transfer of parental label into daughter DNA, indicated that dimers remained in situ in parental chains. (c) Immediately after UV, all parental DNA contained numerous sites sensitive to the extract from M. luteus. 2 h after UV, a portion of parental DNA still contained a number of endonuclease-sensitive (Es) sites, while another portion of parental DNA and all daughter DNA were free of Es sites. (d) The occurrence of parental DNA free of Es sites was not temporally correlated with dimer excision, but with the first round of DNA replication. (e) The amount of DNA free of Es sites corresponded to the amount of replicated DNA. (f) Separation of replicated and unreplicated DNA, and detection of Es sites in both portions separately showed that the replicated DNA was almost free of Es sites, whereas unreplicated DNA contained a number of such sites.

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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%

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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UV-inducible repair II: Its role in various defective mutants of Escherichia coli K-12

Cited by 15 publications

References 26 publications

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

Evidence that dimers remaining in preinduced Escherichia coli B/r Hcr+ become insensitive after DNA replication to the extract from Micrococcus luteus

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

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