Faculty Profile

Lorena Navarro
ASSISTANT PROFESSOR-ACAD YR
Microbiology (College of Biological Sciences)
255 Briggs Hall
Office (530) 752-0260
Lab (530) 752-3641
lonavarro@ucdavis.edu
[Picture of Lorena Navarro]

Degrees:
2002 - PhD - University of California - San Diego - Biology
1993 - BS - University of California - Davis - Biological Sciences

Department and Center Affiliations:
Microbiology

Grad Group Affiliations and Specialties:
Biochemistry and Molecular Biology
Microbiology

Publications:
Navarro, L., Koller, A., Nordfelth, R., Wolf-Watz, H., Taylor, S. and Dixon, J. E. (2007) Identification of a Molecular Target for the Yersinia Protein Kinase A. Molecular Cell, 26(4): 465-477.

Navarro, L., Alto, N. M. and Dixon, J. E. (2005) Functions of the Yersinia Effector Proteins in Inhibiting Host Immune Responses. Current Opinion Microbiol, 8(1): 21-7.

Research Interests:
Our laboratory studies the molecular basis of bacterial pathogenesis in an area of study termed Cellular Microbiology, an exciting and rapidly expanding field that bridges the gap between molecular microbiology and host cellular biology. Our research is focused on studying the virulence mechanisms used by pathogenic bacteria to circumvent the host innate immune response. We are using the Gram-negative bacteria Yersinia as a model system for studying the molecular events occurring at the host-pathogen interface. The genus Yersinia includes important human pathogens causing diseases ranging from the bubonic plague to acute and chronic gastrointestinal disorders. Yersinia employ a sophisticated translocation apparatus, termed the type III secretion system, to deliver bacterial effector proteins directly into the host cytosol where they interfere with eukaryotic signaling pathways and allow the pathogen to evade the host innate immune system, thus favoring survival of the bacteria. We are currently investigating the molecular function and cell biology of an essential Yersinia virulence protein, the Yersinia serine/threonine protein kinase YpkA. Recently, we identified the heterotrimeric G protein, Gaq, as a molecular target for the kinase domain of YpkA. YpkA phosphorylates Gaq at Ser47, a novel phosphorylation site within its GTP binding fold, resulting in reduced affinity of Gaq for GTP, and thus disrupting the ability of Gaq to activate downstream signaling pathways. We are specifically interested in defining the Gaq-mediated downstream signaling events disrupted by YpkA and the contributions these pathways play in host antimicrobial responses. The overall goal of our laboratory is to gain significant molecular insights that will lead to the development of novel strategies to prevent and treat bacterial infectious diseases in humans.

Laboratory Personnel:
Navarro - Ivy Jose