PMID:15721259

Citation	Schlacher, K, Leslie, K, Wyman, C, Woodgate, R, Cox, MM and Goodman, MF (2005) DNA polymerase V and RecA protein, a minimal mutasome. Mol. Cell 17:561-72
Abstract	A hallmark of the Escherichia coli SOS response is the large increase in mutations caused by translesion synthesis (TLS). TLS requires DNA polymerase V (UmuD'2C) and RecA. Here, we show that pol V and RecA interact by two distinct mechanisms. First, pol V binds to RecA in the absence of DNA and ATP and second, through its UmuD' subunit, requiring DNA and ATP without ATP hydrolysis. TLS occurs in the absence of a RecA nucleoprotein filament but is inhibited in its presence. Therefore, a RecA nucleoprotein filament is unlikely to be required for SOS mutagenesis. Pol V activity is severely diminished in the absence of RecA or in the presence of RecA1730, a mutant defective for pol V mutagenesis in vivo. Pol V activity is strongly enhanced with RecA mutants constitutive for mutagenesis in vivo, suggesting that RecA is an obligate accessory factor that activates pol V for SOS mutagenesis.
Links	PubMed Online version:10.1016/j.molcel.2005.01.006
Keywords	Adenosine Triphosphate/metabolism; DNA Damage; DNA Replication/physiology; DNA, Bacterial/genetics; DNA, Bacterial/metabolism; DNA-Directed DNA Polymerase/metabolism; Escherichia coli/enzymology; Escherichia coli/genetics; Escherichia coli Proteins/metabolism; Mutagenesis; Mutation/genetics; Rec A Recombinases/metabolism
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