Targeting Chemosensory Array Formation for Safe Biofilm Dispersal of Pseudomonas aeruginosa

Mentor 1

Sonia Bardy

Start Date

1-5-2020 12:00 AM

Description

Afflicting more than 700,000 people worldwide, Cystic Fibrosis (CF) is a disorder characterized by the buildup of mucus within the airways of affected individuals. Particles such as bacteria get trapped in the airways of CF patients and increase the risk of infection, respiratory failure, and other complications. One such bacteria, Pseudomonas aeruginosa, forms biofilms within the lungs of CF patients. These biofilms have increased antibiotic resistance which hinders treatment of P. aeruginosa infection; biofilm dispersal is proposed as a critical part of treatment of P. aeruginosa infection. However, biofilm dispersal of swimming bacteria can trigger satellite infections within the airways. Safe biofilm dispersion would require non-motile bacteria. Swimming motility, powered by a rotating flagellum, is controlled by a chemotaxis system of P. aeruginosa. Proper swimming motility relies on the formation and localization of unipolar chemosensory arrays. It was recently discovered that interrupting the stability and/or localization of these chemosensory arrays has negative effects on swimming motility. I am seeking to understand the level of interdependence between chemosensory proteins that form these arrays and are essential for swimming motility. Specifically, my results will focus on protein stability in the absence of an interacting partner. I have created fluorescent fusion proteins and will use FACS analysis to determine if protein expression is altered in the absence of an interacting partner. These results will help better model the protein interactions in array formation and signal transduction in P. aeruginosa and allow us to target swimming motility to limit satellite infections during biofilm dispersal.

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May 1st, 12:00 AM

Targeting Chemosensory Array Formation for Safe Biofilm Dispersal of Pseudomonas aeruginosa

Afflicting more than 700,000 people worldwide, Cystic Fibrosis (CF) is a disorder characterized by the buildup of mucus within the airways of affected individuals. Particles such as bacteria get trapped in the airways of CF patients and increase the risk of infection, respiratory failure, and other complications. One such bacteria, Pseudomonas aeruginosa, forms biofilms within the lungs of CF patients. These biofilms have increased antibiotic resistance which hinders treatment of P. aeruginosa infection; biofilm dispersal is proposed as a critical part of treatment of P. aeruginosa infection. However, biofilm dispersal of swimming bacteria can trigger satellite infections within the airways. Safe biofilm dispersion would require non-motile bacteria. Swimming motility, powered by a rotating flagellum, is controlled by a chemotaxis system of P. aeruginosa. Proper swimming motility relies on the formation and localization of unipolar chemosensory arrays. It was recently discovered that interrupting the stability and/or localization of these chemosensory arrays has negative effects on swimming motility. I am seeking to understand the level of interdependence between chemosensory proteins that form these arrays and are essential for swimming motility. Specifically, my results will focus on protein stability in the absence of an interacting partner. I have created fluorescent fusion proteins and will use FACS analysis to determine if protein expression is altered in the absence of an interacting partner. These results will help better model the protein interactions in array formation and signal transduction in P. aeruginosa and allow us to target swimming motility to limit satellite infections during biofilm dispersal.