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Biochimie. 1991 Apr;73(4):479-84.

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

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Groupe d'Etude Mutagénèse et Cancérogénèse, Laboratoire d'Enzymologie, CNRS, Gif-sur-Yvette, France.


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.

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