@article {802,
	title = {Factors Limiting SOS Expression in Log-Phase Cells of Escherichia coli.},
	journal = {J Bacteriol},
	volume = {194},
	year = {2012},
	month = {2012 Oct},
	pages = {5325-33},
	abstract = {In Escherichia coli, RecA-single-stranded DNA (RecA-ssDNA) filaments catalyze DNA repair, recombination, and induction of the SOS response. It has been shown that, while many (15 to 25\%) log-phase cells have RecA filaments, few (about 1\%) are induced for SOS. It is hypothesized that RecA{\textquoteright}s ability to induce SOS expression in log-phase cells is repressed because of the potentially detrimental effects of SOS mutagenesis. To test this, mutations were sought to produce a population where the number of cells with SOS expression more closely equaled the number of RecA filaments. Here, it is shown that deleting radA (important for resolution of recombination structures) and increasing recA transcription 2- to 3-fold with a recAo1403 operator mutation act independently to minimally satisfy this condition. This allows 24\% of mutant cells to have elevated levels of SOS expression, a percentage similar to that of cells with RecA-green fluorescent protein (RecA-GFP) foci. In an xthA (exonuclease III gene) mutant where there are 3-fold more RecA loading events, recX (a destabilizer of RecA filaments) must be additionally deleted to achieve a population of cells where the percentage having elevated SOS expression (91\%) nearly equals the percentage with at least one RecA-GFP focus (83\%). It is proposed that, in the xthA mutant, there are three independent mechanisms that repress SOS expression in log-phase cells. These are the rapid processing of RecA filaments by RadA, maintaining the concentration of RecA below a critical level, and the destabilizing of RecA filaments by RecX. Only the first two mechanisms operate independently in a wild-type cell.},
	issn = {1098-5530},
	doi = {10.1128/JB.00674-12},
	author = {Massoni, Shawn C and Leeson, Michael C and Long, Jarukit Edward and Gemme, Kristin and Mui, Alice and Sandler, Steven J}
}
@article {811,
	title = {UvrD303, a hyperhelicase mutant that antagonizes RecA-dependent SOS expression by a mechanism that depends on its C terminus.},
	journal = {J Bacteriol},
	volume = {191},
	year = {2009},
	month = {2009 Mar},
	pages = {1429-38},
	abstract = {Genomic integrity is critical for an organism{\textquoteright}s survival and ability to reproduce. In Escherichia coli, the UvrD helicase has roles in nucleotide excision repair and methyl-directed mismatch repair and can limit reactions by RecA under certain circumstances. UvrD303 (D403A D404A) is a hyperhelicase mutant, and when expressed from a multicopy plasmid, it results in UV sensitivity (UV(s)), recombination deficiency, and antimutability. In order to understand the molecular mechanism underlying the UV(s) phenotype of uvrD303 cells, this mutation was transferred to the E. coli chromosome and studied in single copy. It is shown here that uvrD303 mutants are UV sensitive, recombination deficient, and antimutable and additionally have a moderate defect in inducing the SOS response after UV treatment. The UV-sensitive phenotype is epistatic with recA and additive with uvrA and is partially suppressed by removing the LexA repressor. Furthermore, uvrD303 is able to inhibit constitutive SOS expression caused by the recA730 mutation. The ability of UvrD303 to antagonize SOS expression was dependent on its 40 C-terminal amino acids. It is proposed that UvrD303, via its C terminus, can decrease the levels of RecA activity in the cell.},
	keywords = {DNA Helicases, DNA, Bacterial, Escherichia coli K12, Escherichia coli Proteins, Gene Expression Regulation, Bacterial, Mutation, Rec A Recombinases, Recombination, Genetic, SOS Response (Genetics), Ultraviolet Rays},
	issn = {1098-5530},
	doi = {10.1128/JB.01415-08},
	author = {Centore, Richard C and Leeson, Michael C and Sandler, Steven J}
}
