RecBCD dependent DNA degradation in recA13 mutant cells is not the basis of their hypersensitivity to this agent.

2.50
Hdl Handle:
http://hdl.handle.net/10541/93026
Title:
RecBCD dependent DNA degradation in recA13 mutant cells is not the basis of their hypersensitivity to this agent.
Authors:
Chovanec, M; Vlasáková, D; Margison, Geoffrey P; Näslund, M; Brozmanová, J
Abstract:
We have examined the hypersensitivity of Escherichia coli recA13 mutant cells to killing by N-methyl-N'-nitro-N-nitro-soguanidine (MNNG) and have shown out that despite MNNG-induced adaptation they remained vastly more sensitive to the cytotoxic effect of this agent than wild type cells. Because this might have been a consequence of a different extent of induction of the adaptive response in the recA13 background, we have measured O6-alkylguanine-DNA alkyltransferase (ATase) activity in extracts of adapted and non-adapted recA13 mutant and wild type cells. Adaptation increased ATase levels by 28- and 34-fold in wild type and recA13 mutant cells, respectively. Thus, the adaptive response was no less inducible in recA13 mutant cells than in wild type cells. This indicates that the extreme sensitivity of recA13 cells to MNNG is not caused by an inability to repair the principal toxic lesions induced in DNA. Low doses of MNNG caused substantial degradation of cellular DNA in recA13 mutant cells but not in the wild type cells. This DNA degradation is shown to be the RecBCD-enzyme dependent. Since recA13 recB21 double mutants were even more sensitive to MNNG than recA single mutants, DNA degradation appears not to be the cause of the MNNG-hypersensitivity in recA13 cells.
Affiliation:
Department of Molecular Genetics, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Citation:
RecBCD dependent DNA degradation in recA13 mutant cells is not the basis of their hypersensitivity to this agent. 1998, 408 (1):19-25 Mutat. Res.
Journal:
Mutation Research
Issue Date:
Jul-1998
URI:
http://hdl.handle.net/10541/93026
PubMed ID:
9678060
Type:
Article
Language:
en
ISSN:
0027-5107
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorChovanec, Men
dc.contributor.authorVlasáková, Den
dc.contributor.authorMargison, Geoffrey Pen
dc.contributor.authorNäslund, Men
dc.contributor.authorBrozmanová, Jen
dc.date.accessioned2010-02-25T11:45:30Z-
dc.date.available2010-02-25T11:45:30Z-
dc.date.issued1998-07-
dc.identifier.citationRecBCD dependent DNA degradation in recA13 mutant cells is not the basis of their hypersensitivity to this agent. 1998, 408 (1):19-25 Mutat. Res.en
dc.identifier.issn0027-5107-
dc.identifier.pmid9678060-
dc.identifier.urihttp://hdl.handle.net/10541/93026-
dc.description.abstractWe have examined the hypersensitivity of Escherichia coli recA13 mutant cells to killing by N-methyl-N'-nitro-N-nitro-soguanidine (MNNG) and have shown out that despite MNNG-induced adaptation they remained vastly more sensitive to the cytotoxic effect of this agent than wild type cells. Because this might have been a consequence of a different extent of induction of the adaptive response in the recA13 background, we have measured O6-alkylguanine-DNA alkyltransferase (ATase) activity in extracts of adapted and non-adapted recA13 mutant and wild type cells. Adaptation increased ATase levels by 28- and 34-fold in wild type and recA13 mutant cells, respectively. Thus, the adaptive response was no less inducible in recA13 mutant cells than in wild type cells. This indicates that the extreme sensitivity of recA13 cells to MNNG is not caused by an inability to repair the principal toxic lesions induced in DNA. Low doses of MNNG caused substantial degradation of cellular DNA in recA13 mutant cells but not in the wild type cells. This DNA degradation is shown to be the RecBCD-enzyme dependent. Since recA13 recB21 double mutants were even more sensitive to MNNG than recA single mutants, DNA degradation appears not to be the cause of the MNNG-hypersensitivity in recA13 cells.en
dc.language.isoenen
dc.subject.meshAdaptation, Biological-
dc.subject.meshAlkyl and Aryl Transferases-
dc.subject.meshDNA Repair-
dc.subject.meshDNA, Bacterial-
dc.subject.meshEscherichia coli-
dc.subject.meshExodeoxyribonuclease V-
dc.subject.meshExodeoxyribonucleases-
dc.subject.meshMethylnitronitrosoguanidine-
dc.subject.meshMutagens-
dc.subject.meshMutation-
dc.subject.meshRec A Recombinases-
dc.titleRecBCD dependent DNA degradation in recA13 mutant cells is not the basis of their hypersensitivity to this agent.en
dc.typeArticleen
dc.contributor.departmentDepartment of Molecular Genetics, Slovak Academy of Sciences, Bratislava, Slovak Republic.en
dc.identifier.journalMutation Researchen
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