Thermal enhancement of ultraviolet mutability in a dnaB uvrA derivative of Escherichia coli B/r: evidence for inducible error-prone repair.
DNA damage triggers coordinate expression of a cluster of diverse functions in  Escherichia coli, including prophage induction, filamentous growth, and "aberrant" reintiation of DNA replication at the chromosomal origin. The "SOS repair" hypothesis proposes that one of these coordinately inducible functions is an error-prone system of DNA repair ("SOS repair") which is responsible for ultraviolet mutagenesis. In dnaB strains, incubation of 42 degrees C stops DNA synthesis and induces lambda prophage and should, therefore, also induce the postulated error-prone repair activity. Thermal posttreatment of a dnaB urvA derivative of E. coli B/r is found to enhance the yield of ultraviolet-light-induced mutations as much as 50-fold, while having no such effect in the dnaB+ parent strain. The results support the SOS repair hypothesis. The possibility is discussed that the inducible repair system is a mutagenic DNA polymerase.
D003090:Coliphages / Q000378:metabolism / Q000528:radiation effects; D004260:DNA Repair; D004307:Dose-Response Relationship, Radiation; D004926:Escherichia coli / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D009154:Mutation; D009268:Nalidixic Acid / Q000494:pharmacology; D011831:Radiation Genetics; D013696:Temperature; D013941:Thymine / Q000378:metabolism; D014466:Ultraviolet Rays
D009268:Nalidixic Acid; D013941:Thymine