In plants, host response to pathogenic microbes is driven both by microbial perception and detection of modified-self. The Xanthomonas campestris effector protein AvrAC/XopAC uridylylates the Arabidopsis BIK1 kinase to dampen basal resistance and thereby promotes bacterial virulence. Here we show that PBL2, a paralog of BIK1, is similarly uridylylated by AvrAC. However, in contrast to BIK1, PBL2 uridylylation is specifically required for host recognition of AvrAC to trigger immunity, but not AvrAC virulence. PBL2 thus acts as a decoy and enables AvrAC detection. AvrAC recognition also requires the RKS1 pseudokinase of the ZRK family and the NOD-like receptor ZAR1, which is known to recognize the Pseudomonas syringae effector HopZ1a. ZAR1 forms a stable complex with RKS1, which specifically recruits PBL2 when the latter is uridylylated by AvrAC, triggering ZAR1-mediated immunity. The results illustrate how decoy substrates and pseudokinases can specify and expand the capacity of the plant immune system.

A highly conserved eukaryotic protein SGT1 binds specifically to the molecular chaperone, HSP90. In plants, SGT1 positively regulates disease resistance conferred by many Resistance (R) proteins and developmental responses to the phytohormone, auxin. We show that silencing of SGT1 in Nicotiana benthamiana causes a reduction in steadystate levels of the R protein, Rx. These data support a role of SGT1 in R protein accumulation, possibly at the level of complex assembly. In Arabidopsis, two SGT1 proteins, AtSGT1a and AtSGT1b, are functionally redundant early in development. AtSGT1a and AtSGT1b are induced in leaves upon infection and either protein can function in resistance once a certain level is attained, depending on the R protein tested. In unchallenged tissues, steady-state AtSGT1b levels are at least four times greater than AtSGT1a. While the respective tetratricopeptide repeat (TPR) domains of SGT1a and SGT1b control protein accumulation, they are dispensable for intrinsic functions of SGT1 in resistance and auxin responses.

In Arabidopsis ecotype Landsberg erecta (L er ), RPP5 confers resistance to the pathogen Peronospora parasitica. RPP5 is part of a clustered multigene family encoding nucleotide binding-leucine-rich repeat (LRR) proteins. We compared 95 kb of DNA sequence carrying the L er RPP5 haplotype with the corresponding 90 kb of Arabidopsis ecotype Columbia (Col-0). Relative to the remainder of the genome, the L er and Col-0 RPP5 haplotypes exhibit remarkable intraspecific polymorphism. The RPP5 gene family probably evolved by extensive recombination between LRRs from an RPP5 -like progenitor that carried only eight LRRs. Most members have variable LRR configurations and encode different numbers of LRRs. Although many members carry retroelement insertions or frameshift mutations, codon usage analysis suggests that regions of the genes have been subject to purifying or diversifying selection, indicating that these genes were, or are, functional. The RPP5 haplotypes thus carry dynamic gene clusters with the potential to adapt rapidly to novel pathogen variants by gene duplication and modification of recognition capacity. We propose that the extremely high level of polymorphism at this complex resistance locus is maintained by frequency-dependent selection. INTRODUCTIONPlant resistance to animal, fungal, bacterial, and viral pathogens often is governed by gene-for-gene interactions between host resistance ( R ) genes and corresponding pathogen avirulence ( Avr ) genes (Crute, 1994). In the absence of matching R genes, Avr gene products presumably enhance pathogen virulence (Collmer, 1998). Different pathogen strains carry different arrays of Avr genes (e.g., Holub and Beynon, 1996), which may indicate some functional redundancy. In crop monocultures, R genes impose strong selection on pathogen Avr genes for mutations to virulence; as a consequence, plant breeders must continuously recruit new R genes from wild relatives. In natural populations that are genetically and spatially more diverse, the evolutionary forces at work are less clear. However, the population dynamics of all plantpathogen systems are strongly influenced by genetic variation in resistance and virulence determinants (Crute, 1994;Simms, 1996). Parallels have been proposed between the evolution of plant R genes and of genes in the major histocompatibility complex (MHC) of vertebrates (Dangl, 1992;Michelmore and Meyers, 1998). It is of major interest, therefore, to understand the molecular basis for the evolution of host-pathogen specificity and to characterize intraspecific natural variation at R gene haplotypes. Interspecific comparisons have been reported elsewhere Thomas et al., 1998).The capacity to adapt rapidly to a broad spectrum of novel pathogen variants imposes a need for a mechanism that generates new R gene alleles. Many R genes are members of gene families residing at complex loci that can carry several distinct pathogen recognition specificities (HammondKosack and Jones, 1997). R genes, therefore, probably evolve novel Avr recognition capacities...