ISSN:
1365-2958
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Biology
,
Medicine
Notes:
In addition to being an essential component of trans-lesion synthesis, the UmuD′C complex is an antagonist of RecA-mediated homologous recombination. When constitutively expressed at an elevated concentration, the UmuD′C complex sensitizes recA+ bacteria to DNA damage, whereas it has no effect on bacteria expressing a RecA [UmuR] protein that overcomes recombination inhibition. Using as a genetic screen enhanced cell killing on mitomycin plates, we isolated novel umuD′ and umuC mutations that restored mitomycin sensitivity to recA D112G [UmuR] bacteria overproducing the UmuD′C complex. The mutations were named [Rin++] because a characterization in a recA+ as well in a recA D112G background showed that they enhanced UmuD′C-promoted recombination inhibition in two assays, conjugational recombination and recombinational repair of palindrome-containing DNA. The [Rin++] mutations affect five amino acids, G25D, S28T, P29L, E35K, and T95R, in UmuD′ and seven, F10L, Y270C, K277E, F287L, F287S, K342Q and F351I, in UmuC. These amino acids might play a key role in the UmuD′C anti-recombination activity. None of the [Rin++] mutations enhanced UmuD′C-promoted mutagenic bypass of UV lesions, in contrast, several lead to a defect in this process. In this study, we discuss a few molecular mechanisms that could account for the recombination and mutagenesis phenotypes of a mutant UmuD′C [Rin++] complex.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1365-2958.2000.01809.x
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