Jean T. Greenberg, University of Chicago

Profile photo of Jean T. Greenberg, expert at University of Chicago

Professor Chicago, Illinois jgreenbe@midway.uchicago.edu Office: (773) 834-1908

Bio/Research

My broad interest is in how organisms adapt to a changing environment. My lab studies this in the context of pathogen-host interactions using the gram negative pathogen Pseudomonas syringae and its interaction with several plants: the non-crop models Arabidopsis thaliana and Nicotiana benthamiana...

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Bio/Research

My broad interest is in how organisms adapt to a changing environment. My lab studies this in the context of pathogen-host interactions using the gram negative pathogen Pseudomonas syringae and its interaction with several plants: the non-crop models Arabidopsis thaliana and Nicotiana benthamiana, and the crop plants tomato and snap beans. In response to infection, plants mount a complex local defense response involving cell suicide, changes at the plasma membrane, the crosslinking of cell wall components, production of antimicrobials and defense gene activation. Some infections also induce a primed state that allows plants to respond faster when a second infection occurs (systemic acquired resistance, SAR). We study how plants regulate their responses to pathogens by (1) using plant mutants that express one or more aspects of the defense response in the absence of pathogens or are compromised for local defense activation or SAR, (2) discovering and tracking the production and movement of novel defense signals and pathogen-derived molecules, and (3) exploiting secreted virulence effector proteins from the pathogen to discover immune components and discern how they are modified. This involves combining genetic analysis with biochemistry and cell biology. On the pathogen side, we are also characterizing how P. syringae uses its type III secretion apparatus and secreted effectors to colonize the surfaces of a leaf, a unique niche. Finally, two newer projects focus on discerning how pathogen effectors post-translationally modify host immune complexes to suppress signaling and exploiting what we learn about P. syringae effectors to study orthologous effectors from human pathogens.

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