Submitted to: Molecular Plant Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/2/2001
Publication Date: N/A
Interpretive Summary: Diseases caused by fungal pathogens are the greatest impediment to grain cereal production worldwide. An economical way of preventing these diseases is through the use of genetic resistance. In oats, hypersensitive cell death at the site of infection is a significant component of defense against the fungal pathogen, Puccinia coronata, the causal agent of oat crown rust. In this report, we demonstrate that hypersensitive cell death is regulated by two distinct signaling pathways. Two new genes were identified. Rds suppresses the hypersensitive response, but not the resistance, mediated by the Pc82 resistance gene. In contrast, Rih confers the hypersensitive response in both resistant and susceptible plants. These results indicate that hypersensitive cell death is not essential for resistance to crown rust. This is the first description of the separation of gene-for-gene resistance from hypersensitive response in a fungal defense response in grain crops. The results described in this manuscript will impact scientists who are working to understand the intricacies of disease defense responses in plants.
Technical Abstract: The Pca crown-rust resistance cluster in diploid Avena confers gene-for-gene specificity to numerous isolates of Puccinia coronata f. sp. avenae. Recombination breakpoint analysis indicates that specificities conferred by the Pca cluster are controlled by at least 5 distinct genes, designated Pc81, Pc82, Pc83, Pc84, and Pc85. Avena plants with the appropriate genotype frequently respond to P. coronata by undergoing hypersensitive cell death at the sites of fungal infection. Autofluorescence of host cells in response to P. coronata occurs in plants that develop visible necrotic lesions, but not in plants that lack this phenotype. Two newly described, non-Pc loci were shown to control hypersensitive cell death. Rds (Resistance dependent suppressor of cell death) suppresses the hypersensitive response, but not the resistance, mediated by the Pc82 resistance gene. In contrast, Rih (Resistance independent hypersensitive cell death) confers HR in both resistant and susceptible plants. Linkage analysis indicates that Rds is unlinked to the Pca cluster, whereas Rih is tightly linked to it. These results indicate that multiple synchronous pathways affect the development of hypersensitive cell death and that HR is not essential for resistance to crown rust. Further characterization of these genes will clarify the relationship between plant disease resistance and localized hypersensitive cell death.