December
2001
, Volume
14
, Number
12
Pages
1,376
-
1,383
Authors
Gong-Xin
Yu
,
1
,
2
Ed
Braun
,
2
and
Roger P.
Wise
1
,
2
,
3
Affiliations
1Interdepartmental Genetics Program, 2Department of Plant Pathology, and 3Corn Insects and Crop Genetics Research, U.S. Department of Agriculture, Agricultural Research Service, Iowa State University, Ames 50011-1020 U.S.A.
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RelatedArticle
Accepted 2 August 2001
Abstract
The Pca crown rust resistance cluster in the diploid Avena genus 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 five 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 (HR), 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.
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ArticleCopyright
The American Phytopathological Society, 2001