Black Spot, Black Death, Black Pearl: the Tales of Bacterial Effectors
Kim Orth is the Earl A. Forsythe chair in biomedical science and professor of molecular biology and biochemistry at UT Southwestern. She is a Howard Hughes Medical Institute investigator and a member of the National Academy of Sciences. Her research focuses on bacterial pathogenesis. Orth graduated from Texas A&M University in 1984 with a B.S. in biochemistry. She went to the UCLA School of Medicine for an M.S. in biological chemistry, and then to University of Texas Southwestern Medical Center for a PhD in biochemistry and molecular biology.
My lab is interested in elucidation the activity of virulence factors from pathogenic bacteria so that we can gain novel molecular insight into eukaryotic signaling systems. The marine bacterium Vibrio parahaemolyticus is the worldwide leading cause of seafood-borne acute gastroenteritis. We are working on the two V. parahaemolyticus type 3 secretion systems (T3SS1 and T3SS2) and their bacterial effectors to understand how signaling systems in the eukaryotic host can be manipulated by these bacterial pathogens. Each of the two T3SSs uses a unique repertoire of effectors to manipulate host signaling. The first T3SS1 is thought to be used maintain V. parahaemolyticus’ survival in the environment, while the second T3SS2 is used for pathogenesis in an animal host. For decades, this pathogen has been studied exclusively as an extracellular bacterium. However, recent studies from our lab have revealed the pathogen’s ability to invade and replicate within host cells using the second T3SS2. These studies have elucidated novel evolutionarily conserved mechanism that used by both host and pathogen. One of these, AMPylation, is an important mechanism used for maintaining homeostasis by all metazoan cells when under stress. Our work at UT Southwestern is accomplished using a broad range of tools, including biochemistry, molecular microbiology, protein chemistry, structural biology, yeast genetics, cell biology and more.
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