Abstract
The metabolic checkpoint kinase mTOR regulates cell functions in response to nutrient availability. mTOR kinase activity is suppressed when cells are starved for nutrients, which results in a decrease in protein translation and an increase in autophagy. It has emerged that mTOR activity is also down regulated during infection of macrophages by pathogenic bacteria, which suggests that activation of host autophagy and suppression of protein translation may provide host benefits during infection. Here we examined mTOR regulation and autophagy during infection by the vacuolar pathogens Legionella pneumophila and Coxiella burnetii. Our results reveal important roles for these pathways in host defense against pathogenic microbes, and uncover novel mechanisms pathogenic microbes have evolved to manipulate these host pathways.
Biography
Dr. Craig Roy studied Microbiology at Michigan State University and earned his PhD in Microbiology and Immunology at Stanford University in 1991. After completing a postdoctoral fellowship in the Department of Molecular Microbiology at Tufts University School of Medicine in 1996 he was appointed as an Assistant Professor in the Department of Molecular Genetics and Microbiology at Stony Brook University. In 1998 Dr. Roy moved to Yale University where he is a Professor and Vice-Chair in the Department of Microbial Pathogenesis. Dr. Roy has received several awards, including the American Society for Microbiology’s oldest and most prestigious prize the Eli Lilly and Company Research Award. His research is focused on determining the molecular and cellular events that enable bacterial pathogens to evade defense mechanisms and replicate inside the host cell by creating specialized vacuoles.