@article {803,
	title = {Mu insertions are repaired by the double-strand break repair pathway of Escherichia coli.},
	journal = {PLoS Genet},
	volume = {8},
	year = {2012},
	month = {2012 Apr},
	pages = {e1002642},
	abstract = {Mu is both a transposable element and a temperate bacteriophage. During lytic growth, it amplifies its genome by replicative transposition. During infection, it integrates into the Escherichia coli chromosome through a mechanism not requiring extensive DNA replication. In the latter pathway, the transposition intermediate is repaired by transposase-mediated resecting of the 5{\textquoteright} flaps attached to the ends of the incoming Mu genome, followed by filling the remaining 5 bp gaps at each end of the Mu insertion. It is widely assumed that the gaps are repaired by a gap-filling host polymerase. Using the E. coli Keio Collection to screen for mutants defective in recovery of stable Mu insertions, we show in this study that the gaps are repaired by the machinery responsible for the repair of double-strand breaks in E. coli-the replication restart proteins PriA-DnaT and homologous recombination proteins RecABC. We discuss alternate models for recombinational repair of the Mu gaps.},
	issn = {1553-7404},
	doi = {10.1371/journal.pgen.1002642},
	author = {Jang, Sooin and Sandler, Steven J and Harshey, Rasika M}
}
@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}
}
