William Dixon ’09
Characterization of the FlpA Protein and Its Role in Flagellar Placement and Pathogenesis of Pseudomonas aeruginosa
Over the summer I worked with the bacteria Pseudomonas aeruginosa in the Gitai lab in Princeton, NJ. P. aeruginosa is a gram-negative bacteria that infects immune-challenged humans as well as many model organisms such as C. elegans. It is most dangerous to humans with cystic fibrosis and severe burn victims. To infect, P. aeruginosa uses flagella, a propeller-like tail, and type IV pili, a shorter structure that functions somewhat like a grappling hook. After initial infection, P. aeruginosa forms biofilms for better growth and increased antibiotic resistance. If the flagella or pili are mislocalized, meaning they are not placed at one of the poles of the bacteria, it has been shown the bacterium has reduced infection strength.
The previous student in the lab where I worked, Natsai Nyakudarika, ran a screen for bacteria with transposon-insertion mutations that affected flagellar function. She looked for bacteria defective in swimming motility, followed by checking these mutants for mislocalization of the protein flhF, a protein responsible for localization of the flagella. She discovered a gene she named flagellar localizing protein A (flpA) that had two mutations responsible for irregular flagellar placement. My goal was to ascertain the role of flpA in flagellar localization.
In the course of my research, I discovered that multiple genes may be responsible for the defect in flagellar placement. My current focus is to identify which genes direct flagellar placement, how they direct flagellar placement, and what their importance in virulence is. I plan on using the C. elegans organism to determine the virulence levels of mutant P. aeruginosa.