Role In SOS Response Research Articles

RecA inactivation as a strategy to reverse the heteroresistance phenomenon in clinical isolates of Escherichia coli

RecA inhibition could be an important strategy to combat resistance because of its key role in SOS response, DNA repair and homologous recombination contributing to bacterial survival. This study evaluates the impact of RecA inactivation on heteroresistance in clinical isolates of Escherichia coli and their corresponding recA-deficient isogenic strains to multiple classes of antimicrobial agents. A high frequency (> 30%) of heteroresistance was observed in this collection of clinical isolates. Deletion of the recA gene led to a marked reduction in heteroresistant subpopulations, especially against quinolones or β-lactams. The molecular basis of heteroresistance was associated with increase in copy number of plasmid-borne resistance genes (case of blaTEM-1B) or tandem gene amplifications (case of qnrA1). Of note, in the absence of the recA gene, the increase in copy number of resistance genes was suppressed. This makes the recA gene a promising target for combating heteroresistance.

Prophage-Encoded Staphylococcal Enterotoxin A: Regulation of Production in Staphylococcus aureus Strains Representing Different Sea Regions.

The present study investigates the nature of the link between the staphylococcal enterotoxin A (SEA) gene and the lifecycle of Siphoviridae bacteriophages, including the origin of strain variation regarding SEA production after prophage induction. Five strains representing three different genetic lines of the sea region were studied under optimal and prophage-induced growth conditions and the Siphoviridae lifecycle was followed through the phage replicative form copies and transcripts of the lysogenic repressor, cro. The role of SOS response on prophage induction was addressed through recA transcription in a recA-disruption mutant. Prophage induction was found to increase the abundance of the phage replicative form, the sea gene copies and transcripts and enhance SEA production. Sequence analysis of the sea regions revealed that observed strain variances were related to strain capacity for prophage induction, rather than sequence differences in the sea region. The impact of SOS response activation on the phage lifecycle was demonstrated by the absence of phage replicative form copies in the recA-disruption mutant after prophage induction. From this study it emerges that all aspects of SEA-producing strain, the Siphoviridae phage and the food environment must be considered when evaluating SEA-related hazards.

Characterization of the double mutant of Deinococcus radiodurans lexA1 and lexA2

LexA and RecA play a crucial role in SOS response in Escherichia coli. In classical SOS response, LexA functions as a repressor to regulate the expression of many genes including RecA after DNA damage occurs. Previous studies showed that LexA1 or LexA2 is not involved in RecA induction in Deinococcus radiodurans. In this study, we constructed a double mutant of lexA1 and lexA2. Results showed that mutation of lexA1 and lexA2 resulted in an apparent decrease in growth rate and an increased resistance to ultraviolet and hydrogen peroxide compared with wild type R1 and two single mutants. However, this double mutant did not exhibit any remarkably increased constitutive expression of RecA under normal conditions, just like wild type R1 and two single mutants, suggesting that neither LexA1 nor LexA2 is involved in the induced expression of RecA. Further transcriptional assay showed that LexA1 and LexA2 together participated in many regulatory pathways involved in cell division, protein synthesis, antioxidant process, transcription regulation and other mechanisms. These results indicate that there should be a new mechanism by which these damage-induced proteins are regulated in D. radiodurans.