Affiliation:
1. Division of Environmental Health, Boston University School of Public Health, Massachusetts 02118.
Abstract
Recovery of aflatoxin B1-induced base substitution mutations in Escherichia coli was almost completely dependent on the presence of the SOS-mutagenesis-enhancing operon mucAB+; the normal E. coli analog, umuDC+, was not sufficient. Yet aflatoxin B1 induced the SOS response, including the umuDC operon, as well as did UV light. Neither preinduction of the SOS response nor the presence of additional copies of umuDC+ allowed the recovery of aflatoxin B1-induced base substitutions. Thus, the premutagenic DNA lesions induced by aflatoxin B1 reveal a functional difference between UmuDC and MucAB. We estimate that in the presence of MucAB the probability that aflatoxin B1-induced DNA lesions will be converted into mutations is increased at least 10-fold.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Reference46 articles.
1. Inducibility of a
gene product required for UV and chemical mutagenesis;Bagg A.;Proc. Natl. Acad. Sci. USA,1981
2. Excretion of an aflatoxin-guanine adduct in the urine of aflatoxin BI-treated rats;Bennett R. A.;Cancer Res.,1981
3. Different efficiency of UmuDC and MucAB proteins in UV light induced mutagenesis in Escherichia coli;Blanco M.;Mol. Gen. Genet.,1986
4. Influence of RecA protein on induced mutagenesis;Blanco M.;Biochimie,1982
5. Mutagenic repair in Escherichia coli. X. The umuC gene product may be required for replication past pyrimidine dimers but not for the coding error in UV-mutagenesis;Bridges B. A.;Proc. Natl. Acad. Sci. USA,1985
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