W388
Dissecting the Genomic Architecture of Puccinia graminis f. sp. tritici – Wheat Interaction

Date: Sunday, January 15, 2017
Time: 4:05 PM
Room: Royal Palm Salon 3-4
Fei He , Kansas State University, Department of Plant Pathology, Manhattan, KS, Manhattan, KS
Wei Wang , Department of Plant Pathology, Kansas State University, Manhattan, KS
Andres Salcedo , Department of Plant Pathology, Kansas State University, Manhattan, KS
William Rutter , Department of Plant Pathology, Kansas State University, Manhattan, KS
Shiaoman Chao , USDA-ARS, Fargo, ND
Katherine Jordan , Kansas State University, Department of Plant Pathology, Manhattan, KS, Manhattan, KS
Alina Akhunova , Kansas State University, Manhattan, KS
Jorge Dubcovsky , University of California, Davis, Davis, CA
Les J Szabo , USDA-ARS Cereal Disease Lab, St Paul, MN
Matthew N. Rouse , USDA-ARS Cereal Disease Lab, St Paul, MN
Eduard Akhunov , Kansas State University, Department of Plant Pathology, Manhattan, KS, Manhattan, KS
Wheat stem rust caused by Puccinia graminis f. sp. tritici (Pgt) can lead to severe yield losses in wheat. The identification of genetic factors in wheat and Pgt that define the outcome of infection (resistance vs. susceptibility) is critical for developing crops with long lasting resistance. In this project, we performed large-scale profiling of the virulence of 125 Pgt isolates (including the Ug99 race group) on the panel of 460 genetically and geographically diverse wheat accessions. A total of 57,500 disease resistance scores were collected and used to investigate the geographic and genomic distribution of resistance and virulence in the host and pathogen populations. Strong geographically structured patterns of wheat resistance and Pgt virulence were detected. GWAS in wheat identified loci conferring resistance against each of the 125 Pgt isolates revealing the complex genetic architecture and evolutionary dynamic of resistance against wheat stem rust. We have used one of the stem rust resistance genes, Sr35, as entry point to search for a Pgt effector recognized by this gene. The whole genome diversity scan of Sr35-virulent and –avirulent Pgt strains including the natural and chemically mutagenized isolates helped to identify a candidate effector gene successfully validated using in planta assays. The effector’s sequence diversity explained most of the virulence of Pgt isolates on the Sr35+ and Sr35- wheat lines. We demonstrate that by applying large-scale phenotyping and whole genome sequencing to the populations of both host and pathogen it is possible to dissect the genetic architecture their interaction.