Control of recA dependent activities in Escherichia coli: a possible role for the recF product.
DNA repair and genetic recombination have been studied in recF143 mutants of Escherichia coli in which expression of inducible, SOS repair activities was altered by additional mutations either in lexA or recA. recF143 and lexA3 appeared to act additively to increase sensitivity to UV irradiation and to reduce recombination proficiency. The recF defect was suppressed in strains carrying the tif-1 allele of recA but not in strains carrying mutations that increased synthesis of recA+ protein or which directly inactivated lexA repressor. These and other data are interpreted to suggest that the recF defect is related to a reduced activity of recA protein. The implications of these findings are discussed in relation to the control of SOS activities and cell division during normal growth.
D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics*; D004260:DNA Repair; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000528:radiation effects; D005798:Genes, Bacterial; D005809:Genes, Regulator; D009154:Mutation; D009582:Nitrofurantoin / Q000494:pharmacology; D011938:Rec A Recombinases; D011995:Recombination, Genetic; D012697:Serine Endopeptidases; D014466:Ultraviolet Rays; D000099160:LexA Repressor Protein
D001426:Bacterial Proteins; D009582:Nitrofurantoin; D011938:Rec A Recombinases; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein