Disease relevance of recA

• Ciprofloxacin treatment resulted in enhanced recA transcription, indicating involvement of the SOS response in phage mobilization [1].
• A genetic and molecular characterization of the recA gene from Staphylococcus aureus [2].
• Next, using Bacillus subtilis recA as a probe, we cloned S. aureus recA and determined its nucleotide sequence [2].

High impact information on recA

• Steady-state levels of recA and fnbB, but not fnbA, mRNA were co-coordinately increased >3-fold in CPX-exposed strain RA1 [3].
• Whereas agr and sarA mutants of RA1 exposed to CPX still displayed increased adhesion to fibronectin, the CPX-triggered response was abolished in the uvs-568 recA mutant, but was restored following complementation with wild type recA [3].
• We conclude that activation of recA and derepression of lexA-regulated genes by CPX may represent a response to drug-induced damage that results in a novel induction of a virulence factor leading to increased bacterial tissue adherence [3].
• It is readily transferred to a recA recipient, and it always inserts into a unique chromosomal copy of the 17 nucleotide sequence in the same orientation [4].
• Mutations were also obtained in recA and lsp (encoding the S. aureus prolipoprotein signal peptidase) [5].

Biological context of recA

• To identify candidate regulatory pathway(s) linking drug exposure to up-regulation of fnbB, we disrupted the global response regulators agr, sarA, and recA in the highly quinolone-resistant strain RA1 [3].
• Although these phenotypes were tentatively attributed to mutations within the S. aureus recA gene, experimental evidence to confirm this has never been reported [2].

Analytical, diagnostic and therapeutic context of recA

• Electrophoretic mobility shift assays revealed specific binding of purified S. aureus SOS-repressor LexA to recA and fnbB, but not to fnbA or rpoB promoters [3].

References