Genetic analysis and dissection of crown rust resistance in diploid Avena

Disease resistance genes provide an effective way to prevent disease. They confer resistance specificity to a variety of plant pathogens, however, they share conserved mechanisms of pathogen recognition and resistance induction. Resistance genes are often organized as clusters in individual plant genomes. The gene clusters are predicted to be a source of genetic diversity for new resistance specificity. A series of 5 tightly linked genes; Pc81, Pc82, Pc83, Pc84 and Pc85 were authenticated within the Pca crown rust resistance cluster by recombination analysis. They conferred resistance specificity to six different crown-rust isolates. Three markers, Agx4, Agx7 and Agx9 were identified by AFLP-based bulk segregant analysis. These markers were tightly linked to the resistance genes within the Pca. Agx4 co-segregates with Pc85. Comparative mapping focused on resistance gene regions would provide clue to determine the orthologous relationship among these genes of different plant species. A set of 21 heterologous probes was mapped on genomes of oat, maize, and barley. The result showed conserved linkage relationships between these markers and a variety of resistance genes on linkage group A of diploid oat, its homoeologous groups in hexaploid oat, chromosome 1H in barley, and chromosomes 3, 6 and 8 in maize. A saturated Avena map was established by AFLP and retrotransposon-based S-SAP analysis. This map consists of 372 AFLP, 79 S-SAP markers and 45 RFLP anchor markers;Localized cell death is one of most important components in the plant disease resistance. Study on the genetic mechanism of the cell death will improve our understanding of plant disease resistance and be a great benefit of Avena crop improvement. The rdh (r&barbelow;esistance d&barbelow;ependent h&barbelow;ypersensitive lesion development) and Rih (R&barbelow;esistance i&barbelow;ndependent h&barbelow;ypersensitive lesion development) loci were identified. They mediate fungus-induced lesion development in response to infection of crown-rust isolates 276 and 290 respectively. Calcofluor staining of infection sites indicated that cell death was involved in the interaction between the plant host cells and the crown-rust fungus in plants with hypersensitive lesion development. The observation indicated that this phenotype was controlled by additional factors