Mutations in uvrD induce the SOS response in Escherichia coli.
We have isolated three new mutations in uvrD that increase expression of the Escherichia coli SOS response in the absence of DNA damage. Like other uvrD (DNA helicase II) mutants, these strains are sensitive to UV irradiation and have high spontaneous mutation frequencies. Complementation studies with uvrD+ showed that UV sensitivity and spontaneous mutator activity were recessive in these new mutants. The SOS-induction phenotype, however, was not completely complemented, which indicated that the mutant proteins were functioning in some capacity. The viability of one of the mutants in combination with rep-5 suggests that the protein is functional in DNA replication. We suggest that these mutant proteins are deficient in DNA repair activities (since UV sensitivity is complemented) but are able to participate in DNA replication. We believe that defective DNA replication in these mutants increases SOS expression.
Ossanna
N
N
Department of Molecular and Cellular Biology, University of Arizona, Tucson 85721.
Mount
D W
DW
D000251:Adenosine Triphosphatases / Q000235:genetics*; D004265:DNA Helicases / Q000235:genetics*; D004260:DNA Repair; D004307:Dose-Response Relationship, Radiation; D004926:Escherichia coli / Q000201:enzymology / Q000235:genetics* / Q000528:radiation effects; D029968:Escherichia coli Proteins; D005838:Genotype; D009154:Mutation; D013014:SOS Response, Genetics; D014466:Ultraviolet Rays
D029968:Escherichia coli Proteins; C506744:rep protein, E coli; D000251:Adenosine Triphosphatases; C506746:UvrD protein, E coli; D004265:DNA Helicases