Characterizing the Role of Sigma Factor Rpoh in the Nitric Oxide Signaling System of Pseudomonas Aeruginosa
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Nitric oxide produced by mammalian cells plays an important role in combating bacterial infections. Nitric oxide induces biofilm dispersion and increases susceptibility to antimicrobials in the opportunistic pathogen P. aeruginosa. However, P. aeruginosa harbors a network of genes that can sense and detoxify nitric oxide and, thus, allow it to survive and cause infection. Preliminary work from my lab shows that the EBP FhpR as well as the -factor RpoH are necessary for nitric oxide sensing and detoxification. Furthermore, our data suggests that these two transcription factors link nitric oxide response to production of the virulence factor pyoverdine. My lab will define the nitric oxide response system of the pathogen P. aeruginosa. In order to accomplish this, we will examine the role of FhpR and RpoH in nitric oxide response. We will identify the targets of these transcription factors using transcriptomics coupled with mutational analysis. We will biochemically characterize each transcription factor, their target gene products, and the signals that activate this pathway. Additionally, we will determine the mechanisms by which FhpR and RpoH regulate production of the virulence factor pyoverdine. Results from this study will show how P. aeruginosa protects itself from nitrosative stress during infections. Understanding the regulatory networks that allow P. aeruginosa to evade host defenses and initiate virulence will help develop new strategies for combating this severe pathogen.
Department of Biology
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