Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta-Galactosidase activities (beta-GA) of E. coli strains carrying the fusion gene of recA and lacZ, GE94 and its DNA repair-deficient derivatives such as KY946[uvrA], KY945[recA] and KY943[lexA] treated with UV, 4NQO, MNNG and MMC were examined. The beta-GA, reflecting the SOS-inducing activity, of GE94 and KY946 treated with these compounds increased significantly with a clear dose-response relationship, and reached a maximum level within 60 min, while no response was seen in KY945 and KY943. Using KY946 and KY945 as a positive and a negative indicator, respectively, the SOS-inducing activity of oxidative mutagens, i.e., hydrogen peroxide (H2O2), formaldehyde, tert-butyl hydroperoxide, cumene hydroperoxide and streptonigrin, was investigated. Clear dose-dependent increases in beta-GA were observed in KY946 treated with all oxidative mutagens tested, but not in KY945. Significant increases in beta-GA were observed with a lower concentration of H2O2 and a shorter incubation time of 4NQO in this assay than in the umu-test. The assay, called 'Rec-lac test' by us, may be useful to detect environmental genotoxic substances.
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PMID:'Rec-lac test' for detecting SOS-inducing activity of environmental genotoxic substance. 189 67

The term 'antimutagen' was originally used to describe an agent that reduces the apparent yield of spontaneous and/or induced mutations, regardless of the mechanisms involved. The 'antimutagens' include 'desmutagens' and 'bio-antimutagens'. In this article, our attention was focused on the bio-antimutagens affecting DNA repair in bacteria. Cobaltous chloride reduced the frequency of mutations in Escherichia coli induced by MNNG. The possibility that metal compound inhibits the growth of mutagen-treated cells was examined. The results clearly showed that the antimutagen surely reduces the mutation rate. The target of cobaltous chloride was found to be cellular factors including Rec A. Vanillin and cinnamaldehyde had strong antimutagenic activities against UV, 4NQO and AF-2. They stimulated Rec A-dependent recombination repair functions in the mutagen-treated cells. Among plant materials, tannins possess antimutagenic activity against UV-induced mutations in E. coli. It has been found that tannic acid stimulates the excision repair encoded by the uvrA gene thereby reducing the yield of mutants. Substances which are antimutagenic in bacterial systems also had antimutagenic activity in cultured mammalian cell systems. Vanillin reduced the frequency of mutagen-induced chromosomal aberrations.
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PMID:Antimutagenesis by factors affecting DNA repair in bacteria. 305 69

DNA lesions may be recognized and repaired by more than one DNA-repair process. If two repair systems with different error frequencies have overlapping lesion specificity and one or both is inducible, the resulting variable competition for the lesions can change the biological consequences of these lesions. This concept was demonstrated by observing mutation in yeast cells (Saccharomyces cerevisiae) exposed to combinations of mutagens under conditions which influenced the induction of error-free recombinational repair or error-prone repair. Total mutation frequency was reduced in a manner proportional to the dose of 60Co-gamma- or 254 nm UV radiation delivered prior to or subsequent to an MNNG exposure. Suppression was greater per unit radiation dose in cells gamma-irradiated in O2 as compared to N2. A rad3 (excision-repair) mutant gave results similar to wild-type but mutation in a rad52 (rec-) mutant exposed to MNNG was not suppressed by radiation. Protein-synthesis inhibition with heat shock or cycloheximide indicated that it was the mutation due to MNNG and not that due to radiation which had changed. These results indicate that MNNG lesions are recognized by both the recombinational repair system and the inducible error-prone system, but that gamma-radiation induction of error-free recombinational repair resulted in increased competition for the lesions, thereby reducing mutation. Similarly, gamma-radiation exposure resulted in a radiation dose-dependent reduction in mutation due to MNU, EMS, ENU and 8-MOP + UVA, but no reduction in mutation due to MMS. These results suggest that the number of mutational MMS lesions recognizable by the recombinational repair system must be very small relative to those produced by the other agents. MNNG induction of the inducible error-prone systems however, did not alter mutation frequencies due to ENU or MMS exposure but, in contrast to radiation, increased the mutagenic effectiveness of EMS. These experiments demonstrate that in this lower eukaryote, mutagen exposure does not necessarily result in a fixed risk of mutation, but that the risk can be markedly influenced by a variety of external stimuli including heat shock or exposure to other mutagens.
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PMID:Inducible DNA-repair systems in yeast: competition for lesions. 354 7

Neocarzinostatin (NCS) produces apurinic/apyrimidinic (AP) sites in DNA which are repaired by the AP excision repair system. Survival after NCS treatment is not determined exclusively by this repair system, presumably because of the production of other, lethal, lesions. MNNG also produces multiple lesions which may be handled by cells in different ways. In E. coli, MNNG treatment results in rapid induction of a system which removes O6-methylguanine. Inhibition of this induction with chloramphenicol results in a large increase in mutation frequency. Induction of an enzyme which removes O6-methylguanine probably accounts for the enrichment of mutations near DNA growing points. MNNG also induces multiple closely linked mutations. The production of multiple mutations but not of single-site mutations is blocked in rec A and uvr E strains. The exact nucleotide site at which DNA synthesis is blocked in vitro by reaction with mutagens can be observed in a phi X174 system in which the nucleotide sequence is known. DNA polymerase I catalyzed synthesis is blocked one nucleotide before the reacted base on the template strand. In contrast, with some damaged templates, AMV reverse transcriptase can insert a base at the level of the reacted nucleotide on the template.
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PMID:Role of cellular systems in modifying the response to chemical mutagens. 645 18

More than 200 mutants of Aspergillus nidulans were isolated as hypersensitive to the monofunctional alkylating agent MNNG and/or UV-irradiation (designated nuv mutants). Of these, 23 were selected for further characterization. All were markedly hypersensitive to both MNNG and the quasi-UV-mimetic mutagen 4-NQO. The hypersensitive phenotype of each mutant was shown to result from mutation of a single gene. The nuv mutants exhibited a diverse range of growth responses on solid media containing various concentrations of MNNG or 4-NQO. This suggested that they represented many nonallelic mutations. Analysis to determine the dominance/recessiveness of the nuv mutations with respect to hypersensitivity revealed that most were fully recessive, although several appeared to be semidominant. A novel system to assay homologous mitotic recombination using simple plating tests was developed. The system was exploited to determine the effects of the nuv mutations on mitotic recombination. Of the 23 mutations tested, 10 caused a hypo-recombination phenotype and three a hyper-recombination phenotype, while 10 appeared to have no effect on recombination. The hypo-rec effect of one of the mutations, nuv-117, appeared to be semidominant. Transcomplementation analysis between seven of the nuv mutations defined at least six nonallelic loci.
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PMID:The isolation of mutagen-sensitive nuv mutants of Aspergillus nidulans and their effects on mitotic recombination. 832 81