Add time:08/25/2019         Source:sciencedirect.com

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.

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