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- W1488968359 abstract "External queues can lead to dramatic changes in host cell signaling. Research in my lab centers around elucidating the biochemical activity of virulence factors, termed effectors, used by bacteria to manipulate eukaryotic signaling machinery. My lab approaches the analysis of host signaling pathways by tapping into the enormous reservoir of bacterial virulence factors that are used by bacterial pathogens to manipulate a eukaryotic cell during infection. Most effectors are predicted to have usurped a eukaryotic activity that is then modified by the pathogen for its own advantage. Gram-negative bacteria use a type III secretion system (T3SS) as a transport vehicle to deliver the virulence factors from the bacterial cytosol to the target host cytosol. The bacterial pathogen Vibrio parahaemolyticus contains two of these systems, T3SS1 and T3SS2, which are believed to function independently of one another in different hosts. The former is found in all Vibrio parahaemolyticus strains and causes death of host cells within hours of infection by induction of autophagy, followed by cell blebbing and rounding with the subsequent release of cellular contents. The other system, T3SS2, is associated with clinical isolates and mediates invasion, followed by vacuolar escape into the cytosol, proliferation and, finally, lysis of the host cells. To uncover the biological mechanisms used by effectors, we use a broad range of tools, including biochemistry, molecular microbiology, biophysics, structural biology, yeast genetics, and cell biology. We have discovered that pathogens utilize novel posttranslational modifications, including Ser/Thr acetylation and AMPylation. We have also uncovered unique mechanisms that manipulate the dynamics of the actin cytoskeleton, the induction of autophagy, and the maintenance of cell membrane integrity. As some of these mechanisms, such as AMPylation, are used by the host, we went on to discover that eukaryotic Fic-mediated AMPylation/deAMPylation on the endoplasmic reticulum chaperone, BiP, serves as a rheostat for the unfolded protein response. Future studies will endeavor to understand other crafty ways that host cells can be manipulated by pathogens. Support or Funding Information HHMI, NIH, Welch Foundation, Once Upon a Time… Foundation This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
- W1488968359 created "2016-06-24" @default.
- W1488968359 creator A5052782883 @default.
- W1488968359 date "2018-04-01" @default.
- W1488968359 modified "2023-09-26" @default.
- W1488968359 title "Black Spot, Black Death, Black Pearl: The Tales of Bacterial Effectors" @default.
- W1488968359 doi "https://doi.org/10.1096/fasebj.2018.32.1_supplement.375.1" @default.
- W1488968359 hasPublicationYear "2018" @default.
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