Poster Session #1
Presentation Type
Poster
Faculty Mentor’s Full Name
Patrick Secor
Faculty Mentor’s Department
Division of health sciences
Abstract / Artist's Statement
A bacteriophage integrase regulates virulence factor production
in Pseudomonas aeruginosa
Pseudomonas aeruginosa is a bacterial pathogen that causes hospital-acquired infections and is very difficult to kill with antibiotics. This is especially true when P. aeruginosa grows as a biofilm—a complex community of bacteria encased in a protective extracellular matrix. P. aeruginosa biofilms produce large amounts of filamentous Pf bacteriophage, which are viruses that infect P. aeruginosa. Pf bacteriophage are known to increase the virulence of P. aeruginosa. However, the underlying mechanisms that cause this are unknown. Our preliminary results suggest that when the Pf bacteriophage integrase gene intP is overexpressed, production of the virulence factor pyocyanin is enhanced. When intP is deleted, pyocyanin production is repressed in P. aeruginosa. Like other bacteriophage integrases, intP inserts bacteriophage DNA into the bacterial chromosome. We hypothesize that intP integrates bacteriophage DNA into bacterial genes that regulate pyocyanin production. To test this hypothesis, we will use genetic approaches to disable the integrase activity of intP followed by biochemical assays to measure pyocyanin production. Understanding how Pf bacteriophage manipulate the virulence of P. aeruginosa may result in new ways to treat or prevent infections caused by this ubiquitous bacterial pathogen.
Category
Life Sciences
A bacteriophage integrase regulates virulence factor production in Pseudomonas aeruginosa
UC South Ballroom
A bacteriophage integrase regulates virulence factor production
in Pseudomonas aeruginosa
Pseudomonas aeruginosa is a bacterial pathogen that causes hospital-acquired infections and is very difficult to kill with antibiotics. This is especially true when P. aeruginosa grows as a biofilm—a complex community of bacteria encased in a protective extracellular matrix. P. aeruginosa biofilms produce large amounts of filamentous Pf bacteriophage, which are viruses that infect P. aeruginosa. Pf bacteriophage are known to increase the virulence of P. aeruginosa. However, the underlying mechanisms that cause this are unknown. Our preliminary results suggest that when the Pf bacteriophage integrase gene intP is overexpressed, production of the virulence factor pyocyanin is enhanced. When intP is deleted, pyocyanin production is repressed in P. aeruginosa. Like other bacteriophage integrases, intP inserts bacteriophage DNA into the bacterial chromosome. We hypothesize that intP integrates bacteriophage DNA into bacterial genes that regulate pyocyanin production. To test this hypothesis, we will use genetic approaches to disable the integrase activity of intP followed by biochemical assays to measure pyocyanin production. Understanding how Pf bacteriophage manipulate the virulence of P. aeruginosa may result in new ways to treat or prevent infections caused by this ubiquitous bacterial pathogen.