Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/13/2000
Publication Date: N/A
Interpretive Summary: Wheat stem rust has a long history of causing major damage to wheat and barley production in North America. Disease losses have been greatly reduced by the introduction of cultivars with stem rust resistance genes and the eradication of the alternate host in the central Great Plains. This form of plant resistance depends on the ability of the host to specifically yrecognize the wheat stem rust pathogen. The pathogen has developed mechanisms to elude recognition, by changing the molecules (elicitors) which are recognized by the host. Changes in the pathogen elicitors have resulted in the development of different races of the wheat stem rust fungus. In order to understand the elicitors and how they are modified to escape recognition, we have crossed isolates of the wheat stem rust fungus and analyzed the genetics for 10 genes involved in the production of the elicitors. In addition, we have begun to develop a genetic map of this organism so that we will be able to clone the genes involved in the production of these elicitors. This research provides basic genetic information on these elicitors and provides genetic markers that will be useful in molecular studies of rust fungal pathogens.
Technical Abstract: Two strains of the wheat stem rust fungus, Puccinia graminis f.sp. tritici, were crossed on barberry, and a single F1 progeny strain further selfed to yield 135 F2 progeny for genetic analysis and mapping of avirulence loci. Parent, F1, and 81 pure F2 progeny strains were examined for avirulent vs. virulent (avr/vir) phenotypes on 46 wheat differential cultivars carrying stem rust resistance (Sr) genes. F2 strains segregated for avr/vir phenotypes on ten wheat Sr differential cultivars. For eight Sr differentials, phenotypic ratios suggest single dominant avirulence genes. Using a new system of nomenclature for stem rust genes that affect avirulence/virulence phenotype, the loci were designated AvrT6, AvrT8a, AvrT9a, AvrT10, AvrT21, AvrT28, AvrT30, and AvrTU. Phenotypic ratios on the Sr; differential of ca. 15:1 suggests an epistatic interaction of two dominant unlinked genes for avirulence phenotype. Avirulence on Sr9d slightly favors a 3:13 over a 1:3 ratio, which could indicate two segregating genes interacting epistatically, one dominant for avirulence on Sr9d and one dominant for avirulence inhibition. Further study is needed to confirm that two genes affect phenotype on Sr9d. Linkage analysis of 279 dominant and 10 codominant RAPD markers, and 181 dominant and 5 codominant AFLP markers, has thus far consolidated markers into 58 linkage groups. DNA markers are linked to each of the 8 single dominant AvrT genes, with the closest linkages between AvrT6 and RAPD marker Xcrl34-155 (5.5 cM) and between AvrT8a and AFLP marker XeAC/mCT-194 (5.8 cM). AvrT genes are on seven linkage groups; AvrT10 and AvrTU are linked to each other at 8.7 cM.