Arabidopsis Mutations at the RPS2 Locus Result in Loss of Resistance to Pseudomonas syringae Strains Expressing the Avirulence Gene avrRpt2. Guo-Liang Yu. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston 02114 U.S.A. Fumiaki Katagiri, and Frederick M. Ausubel. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston 02114 U.S.A. MPMI 6:434-443. Accepted 9 March 1993. Copyright 1993 The American Phytopathological Society.

We isolated and characterized two Arabidopsis thaliana mutants that fail to mount a hypersensitive defense response (HR) when infiltrated with phytopathogenic Pseudomonas strains carrying the avirulence (avr) gene avrRpt2 but still mount an HR when infiltrated with strains carrying other avr genes. One of these mutants was isolated using a method we developed that enriches for Arabidopsis seedlings that survive vacuum-infiltration with a bacterial strain carrying an avr gene. Genetic analysis showed that the phenotypes of both mutants resulted from mutations at a single locus, RPS2. In contrast to the wild type, both rps2 mutants failed to limit the growth of Pseudomonas strains carrying avrRpt2. Heterozygous RPS2/rps2 plants displayed a phenotype intermediate between those of RPS2/RPS2 and rps2/rps2 homozygotes. These experiments show that the wild-type allele at the rps2 locus, RPS2, encodes a component of a signal transduction pathway that responds to a signal generated by avrRpt2 and that RPS2 is required for the elicitation of an HR. RPS2 was mapped near the restriction fragment length polymorphism marker PG11 on chromosome IV.