Our Faculty : Primary Faculty

Gregory V. Plano, Ph.D.

Current Research Interests
Over the past 20 years, Dr. Plano’s has employed Yersinia pestis, the agent of plague, as a model pathogen to investigate basic mechanisms of microbial virulence. Many of these studies have been focused on the type III secretion system (T3SS), a complex nanomachine used by bacterial pathogens to inject anti-host effector proteins into eukaryotic cells. In addition, Dr. Plano has investigated the role of multiple surface-exposed outer membrane proteins in Y. pestis virulence, including the Attachment and Invasion Locus (Ail) protein, the plasminogen activator protease (Pla) and Outer Membrane Protein A (OmpA). Currently, Dr. Plano’s laboratory has two NIH-funded projects that are focused on (i) the characterization of Ail and (ii) two recently identified novel E3 ubiquitin ligase effector proteins (YlrA and YlrC) that Y. pestis injects into host cells. Dr. Plano has also been characterizing the mechanisms by which diverse bacterial pathogens prevent the expression of Perforin-2 by host epithelial and fibroblast cells. All bacterial pathogens examined prevented expression of perforin-2 but non-pathogenic bacteria such as laboratory E. coli or Staphylococcus epidermidis triggered Perforin-2 expression. Dr. Plano has determined that Salmonella enterica employs two distinct stratagies to prevent Perforin-2 expression. First Salmonella extensively modify their LPS to prevent LPS recognition and subsequent TLR4-dependent signaling. In addition, Salmonella, uses its T3SS to deliver an effector protein termed AvrA, to directly block signaling pathways that lead to Perforin-2 expression.

Research Profile
Pubmed Link