The avrRpt2 locus from Pseudomonas syringae pv. tomato causes virulent strains ofP. syringae to be avirulent on some, but not all, lines ofAabidopsis thaliana and Glycine mar (soybean). We determined the DNA sequence of the avrRpt2 locus and identified the avrRpt2 gene as a 768-bp open reading frame encoding a putative 28.2-kDa protein. Deletion analysis and transcription studies provided further evidence that this open reading frame encodes AvrRpt2. We found that the avrRpt2 gene also has avirulence activity in P. syringae pathogens of Phaseous vulgaris (common bean), suggesting that disease resistance genes specific to avrRpt2 are functionally conserved among diverse plant species. The predicted AvrRpt2 protein is hydrophilic and contains no obvious membrane-spanning domains or export signal sequences, and there was no significant similarity of AvrRpt2 to sequences in the GenBank, EMBL, or Swiss PIR data bases. A comparison of the avrRpt2 DNA sequence to nine other P. syringac avinlence genes revealed a highly conserved sequence, GGAACCNA-N14-CCACNNA, upstream of the translation initiation codon. This motif is located 6 to 8 nucleotides upstream of the transcription start site in all four P. syringae avirulence genes for which a transcription start site has been determined, suggesting a role as a binding site for a novel form of RNA polymerase. Regulation ofavrRpt2 was similar to other P. syrmigae avirulence genes; expression was high in minimal medium and low in rich medium and depended on the hrpRS locus and an additional locus at the opposite end of the hrp cluster of P. syringae pv. tomato.

The RPSS and RPMl disease resistance loci of Arabidopsis confer resistance to Pseudomonas syringae strains that carry the avirulence genes avrB and avrRpm7, respectively. We have previously shown that RPS3 and RPMl are closely llnked genetically. Here, we show that RPSS and RPMl are in fact the same gene. We screened a mutagenized Arabldopsls population wlth a R syringae strain carrying avrB and found 12 susceptible mutants. AI112 mutants were also susceptible to an lsogenic strain carrying avrRpml, indlcating a loss of both RPS3 and RPMl functions. No mutants were recovered that lost only RPS3 function. Genetic analysis of four lndependent mutants revealed that the lesions were in RPS3. Thus, a single gene in Arabidopsis confers resistance that is specific to two distinct pathogen avirulence genes-a gene-forgenes interaction. This observation suggests that the RPS3IRPMl gene product can bind multiple pathogen ligands, or alternatively, that lt does not function as a receptor.

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The RPSS and RPMl disease resistance loci of Arabidopsis confer resistance to Pseudomonas syringae strains that carry the avirulence genes avrB and avrRpm7, respectively. We have previously shown that RPS3 and RPMl are closely llnked genetically. Here, we show that RPSS and RPMl are in fact the same gene. We screened a mutagenized Arabldopsls population wlth a R syringae strain carrying avrB and found 12 susceptible mutants. AI112 mutants were also susceptible to an lsogenic strain carrying avrRpml, indlcating a loss of both RPS3 and RPMl functions. No mutants were recovered that lost only RPS3 function. Genetic analysis of four lndependent mutants revealed that the lesions were in RPS3. Thus, a single gene in Arabidopsis confers resistance that is specific to two distinct pathogen avirulence genes-a gene-forgenes interaction. This observation suggests that the RPS3IRPMl gene product can bind multiple pathogen ligands, or alternatively, that lt does not function as a receptor.