Host Inhibition of a Bacterial Virulence Effector Triggers Immunity to Infection

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Science  08 May 2009:
Vol. 324, Issue 5928, pp. 784-787
DOI: 10.1126/science.1169430

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Infections and Defense

Bacteria secrete effectors to suppress immunity in plant and animal hosts resulting in an evolutionary arms race between bacteria and their eukaryotic hosts. One important aspect of plant immunity against bacteria is based on disease resistance protein complexes, which recognize specific bacterial effectors and activate signal transduction. A strain of the bacteria Pseudomonas that infects tomato and Arabidopsis plants injects its effector protein, AvrPtoB, into plant cells. Two plant protein kinases, Fen and Pto, then stimulate disease defense responses that may restrain or halt the infection. Ntoukakis et al. (p. 784) show that the balance between resistance and susceptibility triggered by AvrPtoB is determined by the kinase activity Pto within a disease resistance complex.


Plant pathogenic bacteria secrete effector proteins that attack the host signaling machinery to suppress immunity. Effectors can be recognized by hosts leading to immunity. One such effector is AvrPtoB of Pseudomonas syringae, which degrades host protein kinases, such as tomato Fen, through an E3 ligase domain. Pto kinase, which is highly related to Fen, recognizes AvrPtoB in conjunction with the resistance protein Prf. Here we show that Pto is resistant to AvrPtoB-mediated degradation because it inactivates the E3 ligase domain. AvrPtoB ubiquitinated Fen within the catalytic cleft, leading to its breakdown and loss of the associated Prf protein. Pto avoids this by phosphorylating and inactivating the AvrPtoB E3 domain. Thus, inactivation of a pathogen virulence molecule is one mechanism by which plants resist disease.

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