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A RecA protein mutant deficient in its interaction with the UmuDC complex

1991; Elsevier BV; Volume: 73; Issue: 4 Linguagem: Inglês

10.1016/0300-9084(91)90115-h

1638-6183

Adriana Bailone, Suzanne Sommer, J. Knezˇević, Marie Dutreix, Raymond Devoret,

Carcinogens and Genotoxicity Assessment

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 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.