Abstract
Inhibition of DNA replication in E. coli results in coordinate expression of a cluster of diverse functions, including prophage induction and filamentous growth, many of which are thermally inducible, without inhibition of DNA synthesis, in strains carrying a mutation in the "tif" locus. It has been proposed that one of the inducible functions in this cluster is responsible for the ultraviolet mutability of E. coli. As a test of this hypothesis, the effect of postirradiation temperature elevation on ultraviolet mutability was compared in strains differing by a tif mutation. In a tif(+) strain, raising the temperature to 42 degrees after irradiation did not change the frequency of induced mutations to tryptophan-independence. Similar treatment of a tif-1 strain resulted in as much as a 10-fold increase in the induced mutation yield. Thermal enhancement of ultraviolet mutability in the tif-1 strain was prevented or promoted by agents known to exert parallel effects on thermal induction of lambda prophage in tif lysogens. The results support the hypothesis that ultraviolet mutability in E. coli depends upon an inducible function that is normally expressed only when DNA replication is inhibited.
MeSH Terms
Adenine/pharmacology
Arginine/pharmacology
Culture Media
Cytidine/pharmacology
Dose-Response Relationship, Radiation
Escherichia coli/metabolism,radiation effects
Guanosine/pharmacology
Hot Temperature
Mutation/radiation effects
Radiation Genetics
Tryptophan/metabolism
Ultraviolet Rays
Chemicals
Culture Media
Guanosine
Cytidine
Tryptophan
Arginine
Adenine
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Witkin E M
References (19)
19 references, click to expand
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