A RecA protein mutant deficient in its interaction with the UmuDC complex.
recA1730 is a dominant point mutation preventing SOS mutagenesis. We demonstrate here that: i) RecA1730 fails to produce mutagenesis even though UmuD' is formed, ii) recA1730, when complemented by recA+, can cleave LexA protein and it displays a UmuDC- phenotype in spite of adequate concentrations of matured UmuD' and UmuC proteins, iii) the Mut- phenotype caused by RecA1730 is partially alleviated by MucAB proteins, functional analogs of UmuDC. To explain the mutant phenotype, we postulate that recA1730 impairs a RecA function required for the positioning of the UmuD'C complex within the replisome at the site of lesions.
Bailone
A
A
Groupe d'Etude Mutagénèse et Cancérogénèse, Laboratoire d'Enzymologie, CNRS, Gif-sur-Yvette, France.
Sommer
S
S
Knezević
J
J
Dutreix
M
M
Devoret
R
R
D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism; D004249:DNA Damage; D004259:DNA-Directed DNA Polymerase; D004926:Escherichia coli / Q000235:genetics; D029968:Escherichia coli Proteins; D015964:Gene Expression Regulation, Bacterial; D009154:Mutation; D010641:Phenotype; D011938:Rec A Recombinases / Q000235:genetics*; D013014:SOS Response, Genetics
D001426:Bacterial Proteins; D029968:Escherichia coli Proteins; C068606:mucAB protein, E coli; D011938:Rec A Recombinases; D004259:DNA-Directed DNA Polymerase; C055218:UmuD protein, E coli