Independent deletions of a pathogen-resistance gene in Brassica and Arabidopsis

Plant disease resistance (R) genes confer race-specific resistance to patho gens and are genetically defined on the basis of intra-specific functional polymorphism. Little is known about the evolutionary mechanisms that genera te this polymorphism. Most R loci examined to date contain alternate allele s and/or linked homologs even in disease-susceptible plant genotypes. In co ntrast, the resistance to Pseudomonas syringae pathovar maculicola (RPM1) b acterial resistance gene is completely absent (rpm1-null) in 5/5 Arabidopsi s thaliana accessions that lack RPM1 function. The rpm1-null locus contains a 98-bp segment of unknown origin in place of the RPM1 gene. We undertook comparative mapping of RPM1 and flanking genes in Brassica napus to determi ne the ancestral state of the RPM1 locus. We cloned two B. napus RPM1 homol ogs encoding hypothetical proteins with approximate to 81% amino acid ident ity to Arabidopsis RPM1. Collinearity of genes flanking RPM1 is conserved b etween B, napus and Arabidopsis. Surprisingly, we found four additional B. napus loci in which the flanking marker synteny is maintained but RPM1 is a bsent. These B. napus rpm1-null loci have no detectable nucleotide similari ty to the Arabidopsis rpm1-null allele. We conclude that RPM1 evolved befor e the divergence of the Brassicaceae and has been deleted independently in the Brassica and Arabidopsis lineages. These results suggest that functiona l polymorphism at R gene loci can arise from gene deletions.