Differential effects of cisplatin and MNNG on dna mutants of Escherichia coli
| dc.contributor.author | Calmann, Melissa A. | |
| dc.contributor.author | Marinus, Martin G. | |
| dc.date | 2022-08-11T08:08:54.000 | |
| dc.date.accessioned | 2022-08-23T16:11:25Z | |
| dc.date.available | 2022-08-23T16:11:25Z | |
| dc.date.issued | 2005-09-08 | |
| dc.date.submitted | 2008-08-15 | |
| dc.identifier.citation | Mutat Res. 2005 Oct 15;578(1-2):406-16. <a href="http://dx.doi.org/10.1016/j.mrfmmm.2005.06.030">Link to article on publisher's site</a> | |
| dc.identifier.issn | 0027-5107 (Print) | |
| dc.identifier.doi | 10.1016/j.mrfmmm.2005.06.030 | |
| dc.identifier.pmid | 16144703 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/33160 | |
| dc.description.abstract | DNA mismatch repair (MMR) in mammalian cells or Escherichia coli dam mutants increases the cytotoxic effects of cisplatin and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We found that, unlike wildtype, the dnaE486 (alpha catalytic subunit of DNA polymerase III holoenzyme) mutant, and a DnaX (clamp loader subunits) over-producer, are sensitive to cisplatin but resistant to MNNG at the permissive temperature for growth. Survival of dam-13 dnaN159 (beta sliding clamp) bacteria to cisplatin was significantly less than dam cells, suggesting decreased MMR, which may be due to reduced MutS-beta clamp interaction. We also found an elevated spontaneous mutant frequency to rifampicin resistance in dnaE486 (10-fold), dnaN159 (35-fold) and dnaX36 (10-fold) strains. The mutation spectrum in the dnaN159 strain was consistent with increased SOS induction and not indicative of MMR deficiency. | |
| dc.language.iso | en_US | |
| dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16144703&dopt=Abstract ">Link to article in PubMed</a> | |
| dc.relation.url | http://dx.doi.org/10.1016/j.mrfmmm.2005.06.030 | |
| dc.subject | Cisplatin; DNA Repair; DNA, Bacterial; Dose-Response Relationship, Drug; Drug Resistance, Microbial; Escherichia coli; Genes, Bacterial; Methylnitronitrosoguanidine; Mutagens; *Mutation; Rifampin; Temperature | |
| dc.subject | Life Sciences | |
| dc.subject | Medicine and Health Sciences | |
| dc.title | Differential effects of cisplatin and MNNG on dna mutants of Escherichia coli | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Mutation research | |
| dc.source.volume | 578 | |
| dc.source.issue | 1-2 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/gsbs_sp/170 | |
| dc.identifier.contextkey | 580022 | |
| html.description.abstract | <p>DNA mismatch repair (MMR) in mammalian cells or Escherichia coli dam mutants increases the cytotoxic effects of cisplatin and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We found that, unlike wildtype, the dnaE486 (alpha catalytic subunit of DNA polymerase III holoenzyme) mutant, and a DnaX (clamp loader subunits) over-producer, are sensitive to cisplatin but resistant to MNNG at the permissive temperature for growth. Survival of dam-13 dnaN159 (beta sliding clamp) bacteria to cisplatin was significantly less than dam cells, suggesting decreased MMR, which may be due to reduced MutS-beta clamp interaction. We also found an elevated spontaneous mutant frequency to rifampicin resistance in dnaE486 (10-fold), dnaN159 (35-fold) and dnaX36 (10-fold) strains. The mutation spectrum in the dnaN159 strain was consistent with increased SOS induction and not indicative of MMR deficiency.</p> | |
| dc.identifier.submissionpath | gsbs_sp/170 | |
| dc.contributor.department | Department of Biochemistry and Molecular Pharmacology | |
| dc.contributor.department | Graduate School of Biomedical Sciences | |
| dc.source.pages | 406-16 |
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