Altered SOS induction associated with mutations in recF, recO and recR.
The SOS system of Escherichia coli aids survival following damage to DNA by promoting DNA repair while cell division is delayed. Induction of the SOS response is dependent on RecA and also on the product of recF. We show that normal induction also requires the products of recO and recR. SOS induction was monitored using a sfiA-lacZ fusion strain. Induction was delayed to a similar degree by mutation in recF, recO or recR. A similar effect was observed following overexpression of RecR from a recombinant recR+ plasmid. We show that the overexpression of RecR also reduces the UV resistance of a recBC sbcBC strain and of a sfiA strain, but not of a rec+sfiA+ strain. The implications of these data for the kinetics of DNA repair are discussed.
Whitby
M C
MC
Department of Genetics, University of Nottingham, Queens Medical Centre, UK.
Lloyd
R G
RG
D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics*; D001483:Base Sequence; D004268:DNA-Binding Proteins / Q000235:genetics*; D004926:Escherichia coli / Q000235:genetics*; D029968:Escherichia coli Proteins; D015964:Gene Expression Regulation, Bacterial; D008969:Molecular Sequence Data; D009154:Mutation; D011836:Radiation Tolerance / Q000235:genetics; D011994:Recombinant Proteins / Q000096:biosynthesis; D013014:SOS Response, Genetics / Q000235:genetics*; D014466:Ultraviolet Rays
D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins; C081006:RecO protein, E coli; C489318:RecR protein, E coli; D011994:Recombinant Proteins; C489340:recF protein, E coli; C065831:RecR protein, Bacteria; C066218:recF protein, Bacteria