| "Bacterial
pathogens deliver type III effector proteins into the plant cell during
infection. On susceptible (r) hosts, type IIIeffectors can contribute to
virulence. Some trigger the action of specific disease resistance (R) gene
products. Theactivation of R proteins can occur indirectly via modification
of a host target. Thus, at least some type III effectors arerecognized at
site(s) where they may act as virulence factors. These data indicate that
a type III effector's host target mightbe required for both initiation of
R function in resistant plants and pathogen virulence in susceptible plants.
In Arabidopsisthaliana, RPM1-interacting protein 4 (RIN4) associates with
both the Resistance to Pseudomonas syringae pv maculicola 1(RPM1) and Resistance
to P. syringae 2 (RPS2) disease resistance proteins. RIN4 is posttranslationally
modified afterdelivery of the P. syringae type III effectors AvrRpm1, AvrB,
or AvrRpt2 to plant cells. Thus, RIN4 may be a target forvirulence functions
of these type III effectors. We demonstrate that RIN4 is not the only host
target for AvrRpm1 and AvrRpt2in susceptible plants because its elimination
does not diminish their virulence functions. In fact, RIN4 negatively regulatesAvrRpt2
virulence function. RIN4 also negatively regulates inappropriate activation
of both RPM1 and RPS2. Inappropriateactivation of RPS2 is nonspecific disease
resistance 1 (NDR1) independent, in contrast with the established requirement
forNDR1 during AvrRpt2-dependent RPS2 activation. Thus, RIN4 acts either
cooperatively, downstream, or independently ofNDR1 to negatively regulate
RPS2 in the absence of pathogen. We propose that many P. syringae type III
effectors havemore than one target in the host cell. We suggest that a limited
set of these targets, perhaps only one, are associated with Rproteins. Thus,
whereas any pathogen virulence factor may have multiple targets, the perturbation
of only one is necessaryand sufficient for R activation." |