@article {823,
	title = {Measurement of SOS expression in individual Escherichia coli K-12 cells using fluorescence microscopy.},
	journal = {Mol Microbiol},
	volume = {53},
	year = {2004},
	month = {2004 Sep},
	pages = {1343-57},
	abstract = {Many recombination, DNA repair and DNA replication mutants have high basal levels of SOS expression as determined by a sulAp-lacZ reporter gene system on a population of cells. Two opposing models to explain how the SOS expression is distributed in these cells are: (i) the {\textquoteright}Uniform Expression Model (UEM){\textquoteright} where expression is evenly distributed in all cells or (ii) the {\textquoteright}Two Population Model (TPM){\textquoteright} where some cells are highly induced while others are not at all. To distinguish between these two models, a method to quantify SOS expression in individual bacterial cells was developed by fusing an SOS promoter (sulAp) to the green fluorescent protein (gfp) reporter gene and inserting it at attlambda on the Escherichia coli chromosome. It is shown that the fluorescence in sulAp-gfp cells is regulated by RecA and LexA. This system was then used to distinguish between the two models for several mutants. The patterns displayed by priA, dnaT, recG, uvrD, dam, ftsK, rnhA, polA and xerC mutants were explained best by the TPM while only lexA (def), lexA3 (ind-) and recA defective mutants were explained best by the UEM. These results are discussed in a context of how the processes of DNA replication and recombination may affect cells in a population differentially.},
	keywords = {Adenosine Triphosphatases, DNA Damage, DNA Helicases, DNA Repair, Escherichia coli K12, Escherichia coli Proteins, Gene Expression Regulation, Bacterial, Genes, Reporter, Microscopy, Fluorescence, Models, Genetic, Promoter Regions, Genetic, Recombinant Fusion Proteins, SOS Response (Genetics), Ultraviolet Rays},
	issn = {0950-382X},
	doi = {10.1111/j.1365-2958.2004.04225.x},
	author = {McCool, Jesse D and Long, Edward and Petrosino, Joseph F and Sandler, Hilary A and Rosenberg, Susan M and Sandler, Steven J}
}
@article {570,
	title = {Geobacter sulfurreducens has two autoregulated lexA genes whose products do not bind the recA promoter: differing responses of lexA and recA to DNA damage.},
	journal = {J Bacteriol},
	volume = {185},
	year = {2003},
	month = {2003 Apr},
	pages = {2493-502},
	abstract = {The Escherichia coli LexA protein was used as a query sequence in TBLASTN searches to identify the lexA gene of the delta-proteobacterium Geobacter sulfurreducens from its genome sequence. The results of the search indicated that G. sulfurreducens has two independent lexA genes designated lexA1 and lexA2. A copy of a dinB gene homologue, which in E. coli encodes DNA polymerase IV, is present downstream of each lexA gene. Reverse transcription-PCR analyses demonstrated that, in both cases, lexA and dinB constitute a single transcriptional unit. Electrophoretic mobility shift assays with purified LexA1 and LexA2 proteins have shown that both proteins bind the imperfect palindrome GGTTN(2)CN(4)GN(3)ACC found in the promoter region of both lexA1 and lexA2. This sequence is also present upstream of the Geobacter metallireducens lexA gene, indicating that it is the LexA box of this bacterial genus. This palindrome is not found upstream of either the G. sulfurreducens or the G. metallireducens recA genes. Furthermore, DNA damage induces expression of the lexA-dinB transcriptional unit but not that of the recA gene. However, the basal level of recA gene expression is dramatically higher than that of the lexA gene. Likewise, the promoters of the G. sulfurreducens recN, ruvAB, ssb, umuDC, uvrA, and uvrB genes do not contain the LexA box and are not likely to bind to the LexA1 or LexA2 proteins. G. sulfurreducens is the first bacterial species harboring a lexA gene for which a constitutive expression of its recA gene has been described.},
	keywords = {Amino Acid Sequence, Bacterial Proteins, Consensus Sequence, DNA Damage, DNA Polymerase beta, DNA Repair, DNA-Binding Proteins, Electrophoretic Mobility Shift Assay, Gene Expression, Genes, Bacterial, Molecular Sequence Data, Promoter Regions, Genetic, Proteobacteria, Rec A Recombinases, Sequence Alignment, Serine Endopeptidases, Transcription, Genetic},
	issn = {0021-9193},
	author = {Jara, M{\'o}nica and N{\'u}{\~n}ez, Cinthia and Campoy, Susana and Fern{\'a}ndez de Henestrosa, Antonio R and Lovley, Derek R and Barb{\'e}, Jordi}
}
@article {841,
	title = {RecOR suppression of recF mutant phenotypes in Escherichia coli K-12.},
	journal = {J Bacteriol},
	volume = {176},
	year = {1994},
	month = {1994 Jun},
	pages = {3661-72},
	abstract = {The recF, recO, and recR genes form the recFOR epistasis group for DNA repair. recF mutants are sensitive to UV irradiation and fail to properly induce the SOS response. Using plasmid derivatives that overexpress combinations of the recO+ and recR+ genes, we tested the hypothesis that high-level expression of recO+ and recR+ (recOR) in vivo will indirectly suppress the recF mutant phenotypes mentioned above. We found that overexpression of just recR+ from the plasmid will partially suppress both phenotypes. Expression of the chromosomal recO+ gene is essential for the recR+ suppression. Hence we call this RecOR suppression of recF mutant phenotypes. RecOR suppression of SOS induction is more efficient with recO+ expression from a plasmid than with recO+ expression from the chromosome. This is not true for RecOR suppression of UV sensitivity (the two are equal). Comparison of RecOR suppression with the suppression caused by recA801 and recA803 shows that RecOR suppression of UV sensitivity is more effective than recA803 suppression and that RecOR suppression of UV sensitivity, like recA801 suppression, requires recJ+. We present a model that explains the data and proposes a function for the recFOR epistasis group in the induction of the SOS response and recombinational DNA repair.},
	keywords = {Bacterial Proteins, Base Sequence, DNA Damage, DNA Repair, DNA-Binding Proteins, Epistasis, Genetic, Escherichia coli, Escherichia coli Proteins, Models, Genetic, Molecular Sequence Data, Phenotype, Plasmids, SOS Response (Genetics), Suppression, Genetic, Ultraviolet Rays},
	issn = {0021-9193},
	author = {Sandler, S J and Clark, A J}
}
