Preliminary data from our laboratory had implicated the involvement of polyphosphate kinase (ppk) in the formation and resuscitation of antibiotic-tolerant persister cells of Pseudomonas aeruginosa PA14. This phenotype was assessed by generating a ppk knockout mutant, as well as a ppk-overexpressing mutant. To further characterize the impact these mutations had on the phenotype of P. aeruginosa, motility assays, as well as growth rate assessment, biofilm formation, oxidative stress tolerance, and virulence assays were carried out. Viable counts after antibiotic challenge revealed increased cell recovery in ppk knockout mutants. Additional phenotypic assay data did not entirely correlate with that previously published for ppk mutant of P. aeruginosa PAO1. Neither biofilm formation, nor susceptibility to peroxides was impacted by the mutation. Swarming and swimming motility assays showed a significant decrease and a significant increase, respectively, by the knockout strain. Implications of these findings are discussed in the context of applying single-strain phenotypic data to the entire species, and additional work is proposed to understand the full extent of polyphosphate regulation.
|Commitee:||Fiumera, Heather L., Schertzer, Jeffrey W.|
|School:||State University of New York at Binghamton|
|School Location:||United States -- New York|
|Source:||MAI 53/04M(E), Masters Abstracts International|
|Keywords:||Biofilm, Persister cells, Polyphosphate, Polyphosphate kinase, Pseudomonas aeruginosa|
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