Themolecular dynamic of genetic recombination in Pseudomonas aeruginosa is the main focus of our research due to itsrole in this bacteria´s capacity to resist treatment during chronic infections.We have results indicating the existence of both RecA dependent and independentpathways coexisting in this species, and intend to determine the factors thatmediate the latter. In order to accomplish such objective we selected a numberof mutant strains corresponding to factors with known/suspected involvement inrecombination, including the radAmutant whose Archaea and E.coli homologueshave recombinase and helicase functions respectively.  Using a genetic system previously developedin our lab, we were able to determine the in vivo recombination rates forseveral mutant strains. In particular, radAmutant showed recombination rates as low as the ones observed in recA mutants(about 200 fold decrease compared to the wt strain). Also, when analyzing the β-galactosidase activityof recombinant clones, we found that the levels of mutagenesis previouslyobserved in the wt and other strains disappear in absence of the RadA protein.

 When the radAstrain was tested in a cisplatin sensibility assay it presented higher levelsof sensibility than the wt strain.  Theseresults indicate that RadA plays a key role in the recombination mechanisms of P. aeruginosa, unknown until now. We arecurrently studying the in vitro function and properties of RadA; as well as thedynamics between it and the main recombination motor, RecA.