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Uridylylation of PBL2 triggers plant immune responses

Uridylylating activity of a plant pathogen inhibits one form of the plant immune response but triggers another. In plants, pathogens induce pattern-triggered immunity (PTI) by activating pattern-recognition receptors on the cell surface and effector-triggered immunity (ETI) by activating intracellular Nod-like receptors (NLRs). Some NLRs initiate ETI upon direct binding to a pathogen effector, whereas other NLRs initiate ETI indirectly by binding to a host protein that has been modified by a pathogen effector. AvrAC is an effector protein of the pathogenic bacterium Xanthomonas campestris that is important for virulence because it inhibits PTI by uridylylating the Arabidopsis thaliana cytoplasmic receptor-like kinase BIK1, a critical component of cell surface receptor complexes that initiate PTI. However, Wang et al. found that plants have a strategy through which the uridylylating activity of AvrAC triggers ETI. AvrAC uridylylated Arabidopsis PBL2, which is closely related to BIK1. Through a combination of genetic and biochemical experiments, the authors determined that AvrAC-mediated uridylylatation of PBL2 caused the recruitment of PBL2 to a preformed complex containing the NLR ZAR1 and the pseudokinase RKS1. The kinase activity of PBL2 was not required for AvrAC-mediated uridylylation of PBL2, for AvrAC-induced binding of PBL2 to ZAR1, or induction of ETI. Whereas AvrAC-mediated modification of BIK1 dampens the host immune response to promote virulence, AvrAC-mediated modification of PBL2 allows the host to initiate ETI. ZAR1 also forms complexes with the RKS1-related pseudokinase ZED1 and initiates ETI when ZED1 is acetylated by an effector protein of Pseudomonas syringae. The findings of Wang et al. expand the known repertoire of mechanisms by which a single NLR can indirectly detect the presence of multiple pathogens by cooperating with different binding partners (see Innes). G. Wang, B. Roux, F. Feng, E. Guy, L. Li, N. Li, X. Zhang, M. Lautier, M.-F. Jardinaud, M. Chabannes, M. Arlat, S. Chen, C. He, L. D. Noël, J.-M. Zhou, The decoy substrate of a pathogen effector and a pseudokinase specify pathogen-induced modified-self recognition and immunity in plants. Cell Host Microbe 18, 285–295 (2015). [PubMed] R. W. Innes, Exploiting combinatorial interactions to expand NLR specificity. Cell Host Microbe 18, 265–267 (2015). [PubMed]