|WILK, AARON - Westmont College
|MCHARGUE, BRITTANY - Westmont College
|BONENFANT, GASTON - Westmont College
|RAMIREZ, JOSE - Westmont College
|JULIO, STEVE - Westmont College
Submitted to: American Society for Microbiology General Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 5/1/2014
Publication Date: 8/1/2014
Citation: Wilk, A., Mchargue, B., Nicholson, T.L., Bonenfant, G., Ramirez, J., Julio, S. 2014. A role for the sensor kinase PlrS in controlling the response of Bordetella bronchiseptica to increased CO2 levels. 114th General Meeting of the American Society for Microbiology. Paper No. 346. p. 189.
Technical Abstract: The ability of Bordetella bronchiseptica to colonize the rodent respiratory tract requires the sensor kinase PlrS, which is presumably part of a two-component regulatory system. Microarray analysis revealed that PlrS influences the expression of several genes required for virulence, including those involved in adherence, resistance to immune functions, and type III secretion. Interestingly, many of the genes in the PlrS regulon were identified in separate microarray experiments as belonging to a CO2-responsive regulon (Hester et al., PLOS One, 7(10), 2012). We characterized the ability of PlrS to influence the CO2-dependent response in B. bronchiseptica strain RB50, and show that the ability of bacteria to adhere to L2 rat epithelial cells and RAW 264 macrophage-like cells is dependent on PlrS when the bacteria were grown in 5% CO¬2. Additionally, the production of several immune-responsive antigens was altered in a PlrS-dependent manner when bacteria were grown in 5% CO2, suggesting that PlrS controls the production of proteins important during infection. Next, we characterized the role of PlrS in strain JC100, which belongs to a group of B. bronchiseptica strains that produce adenylate cyclase toxin (CyaA) only under conditions of elevated CO2. In this strain, CyaA-dependent hemolysis requires intact PlrS. and analogous to strain RB50, adherence to epithelial and macrophage-like cells when bacteria are grown in the presence of 5% CO2 is a PlrS-dependent phenotype. Moreover, a JC100 plrS in-frame deletion mutant is defective in colonizing the rat trachea, demonstrating the importance of plrS for JC100-mediated infection of the rat respiratory tract. Together, our data suggest a role for PlrS in controlling the expression of genes in response to elevated CO2 levels in multiple B. bronchiseptica strains. plrS may allow bacteria to sense and respond appropriately to particular spatial or temporal cues in the respiratory tract, since CO2 is likely an important environmental signal encountered during infection.