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Open Forum on Cell Signaling

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Highlights from Minisymposium 4: Host-Pathogen Interactions and Innate Immunity

10 December 2007

Nancy R. Gough

I attended four of the talks at this minisymposium on Sunday, 2 December 2007. Joanne Engel (UCSF) described how Exotoxin T (ExoT) from Pseudomonas aeruginosa contributes to virulence. ExoT, which has a domain with GTPase-activating protein (GAP) activity and a domain with ADP ribosyltransferase (ADPRT) activity, is injected into the host cell by the type III secretion system. The GAP domain acts through Rho, Rac, and Cdc42 to cause rounding of the infected epithelial cells. The ADPRT domain ADP ribosylates the adaptors Crk I and Crk II, inactivating their SH2 domains, which causes the cells to lose adherence to the substrate. In addition to the morphological changes, infected cells also exhibit a block in cytokinesis. Analysis of the mechanism by which the ADPRT domain of ExoT inhibited cytokinesis revealed the presence of a focal adhesion-like structure at the midbody. ExoT-infected cells fail to recruit syntaxin to this midbody structure, which blocks cytokinesis.

The remaining three talks that I attended highlighted mechanisms by which plant pathogens interact with their hosts or the plant defense response. Xinyan Li of the lab of Mary Beth Mudgett (Stanford) described an atypical receptor-like kinase (RLK) from tomato that appears to be the target of the virulence protein XopN of Xanthomonas campestris pathovar vesicatoria (Xcv). XopN has multiple α-helical repeats. The N-terminal region interacted with tomato atypical RLK (TARK1), which in vitro had very low kinase activity. TARK1 is missing two critical conserved residues that are important for kinase activity. The C-terminal region of XopN interacted with 14-3-3 proteins. Knockout of TARK1 resulted in termination of the apical meristem, thus this protein may have roles in plant defense and development.

Silke Robatzek (Max Planck Institute for Plant Breeding Research) described her work on the subcellular trafficking of the flagellin receptor FLS2. FLS2 bound to the flagellin peptide Flg22 interacted with BAK1 (brassinosteroid insensitive 1-associated receptor kinase 1), and the cells respond with ion flux, production of reactive oxygen species (ROS), and changes in gene expression. In the presence of BAK1, Flg22 triggers the endocytosis of FLS2 in epidermis and leaf mesophyll. Dr. Robatzek found that some mutations of FLS2 that prevented endocytosis prevented ROS production and some did not block ROS production. Endocytosis of FLS2 appears to involve phosphorylation and ubiquitination. The virulence factor AvrPtoB from Pseudomonas syringae pathovar tomato interacts with FLS2 and this interaction is enhanced in the presence of flagellin. How this virulence factor influence FLS2 function and endocytosis remain open questions. See the Editors' Choice for a summary of some of the published work.

Ho Won Jung of the lab of Jean Greenberg (University of Chicago) described a small molecule, azelaic acid, that was isolated from infected Arabidopsis petioles. Leaves sprayed or injected with this small molecule conferred resistance to infection to nontreated leaves, suggesting that azelaic acid may be a mobile signal or may stimulate the production of a mobile signal involved in systemic acquired resistance.

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