Rds and Rih mediate hypersensitive cell death independent of gene-for-generesistance to the oat crown rust pathogen Puccinia coronata f. sp avenae

The Pca crown rust resistance cluster in the diploid Avena genus confers ge ne-for-gene specificity to numerous isolates of Puccinia coronata f. sp. av enae. Recombination breakpoint analysis indicates that specificities confer red by the Pca cluster are controlled by at least five distinct genes, desi gnated Pc81, Pc82, Pc83, Pc84, and Pc85. Avena plants with the appropriate genotype frequently respond to P. coronata by undergoing hypersensitive cel l death at the sites of fungal infection. Autofluorescence of host cells in response to P. coronata occurs in plants that develop visible necrotic les ions but not in plants that lack this phenotype. Two newly described, non-P c loci were shown to control hypersensitive cell death. Rds (resistance-dep endent suppressor of cell death) suppresses the hypersensitive response (HR ), but not the resistance, mediated by the Pc82 resistance gene. In contras t, Rih (resistance-independent hypersensitive cell death) confers HR in bot h resistant and susceptible plants. Linkage analysis indicates that Rds is unlinked to the Pca cluster, whereas Rih is tightly linked to it. These res ults indicate that multiple synchronous pathways affect the development of hypersensitive cell death and that HR is not essential for resistance to cr own rust. Further characterization of these genes will clarify the relation ship between plant disease resistance and localized hypersensitive cell dea th.