Molecular function of PA14_00800 and PrlC and in signaling pathways in the opportunistic pathogen Pseudomonas aeruginosa

• Grant number: 17/24819-0
• Support Opportunities: Scholarships abroad - Research
• Start date: January 15, 2018
• End date: January 14, 2019
• Field of knowledge: Biological Sciences - Biochemistry - Molecular Biology
• Principal Investigator: Regina Lúcia Baldini
• Grantee: Regina Lúcia Baldini
• Host Investigator: Joanne Engel
• Host Institution: Instituto de Química (IQ). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Institution abroad: University of California, San Francisco (UCSF), United States

Abstract

Every living organism coordinates its functions by receiving information from the environment and using them to adjust the pathways that allow its survival and adaptation. As in all cells, bacterial signaling and response systems must be finely regulated to guarantee their success in specific situations. Whereas some bacteria have limited niches, Pseudomonas aeruginosa is the hallmark of an opportunistic organism. It inhabits diverse settings, uses several carbon and energy sources and is capable of synthesizing compounds that provide competitive advantage relative to other microorganisms. P. aeruginosa presents intricate cell-cell signaling systems, intrinsic antibiotic resistance mechanisms and can live in communities referred to as biofilms. This bacterium is often associated to nosocomial infections and causes both acute and chronic pneumonia in cystic fibrosis patients. With roughly 20% of its large genome dedicated to regulate gene expression, P. aeruginosa has been extensively studied regarding many facets of its physiology, but many of its signal transduction pathways are still poorly or uncharacterized. This proposal aims to enhance the knowledge on these signaling pathways that may be targets to efficiently prevent and treat P. aeruginosa infections. Specifically, we intend to disclose the molecular functions of the proteins PrlC and PA14_00800, whose expression is influenced by c-di-GMP levels and that may be part of the Chp transduction pathway, which is associated with surface contact recognition, activating cell motility and expression of virulence genes. (AU)