Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 7/1/2008
Publication Date: 8/17/2008
Citation: Friesen, T.L., Liu, Z., Zhang, Z., Solomon, P.S., Oliver, R.P., Faris, J.D. 2008. Characterization of the role of host-selective toxins in the stagonospora nodorum - wheat pathosystem shows an inverse gene-for-gene structure. 7th Mycosphaerella Stagonospora Symposium in Ascona, Switzerland, August 18-22, 2008. Interpretive Summary:
Technical Abstract: Stagonospora nodorum blotch caused by S. nodorum (teleomorph Phaeosphaeria nodorum) is a devastating disease of wheat that causes significant yield and quality losses worldwide. Although this disease is a major concern for breeders, it has been difficult to characterize the interaction due to its quantitative nature. Our approach has been to use wheat mapping populations segregating for quantitative disease resistance to assist in the identification, purification, and characterization of virulence factors (e.g. host-selective toxins) produced by S. nodorum. The identified host-selective toxins (HSTs) are partially purified and the genes governing sensitivity to individual HSTs are located to wheat chromosomal regions using molecular markers. Once a gene conferring HST sensitivity has been mapped, the effects of a compatible host-toxin interaction (i.e. the presence of the host allele conferring sensitivity and the corresponding HST) is evaluated using QTL analysis to determine the significance of the interaction in disease development induced by the fungus. To date, we have used several wheat mapping populations to identify more than 15 toxin sensitivity loci, which map to different locations in the wheat A, B, and D genomes. Genetic characterization of several host-toxin interactions indicates that some HSTs are major virulence factors with highly significant roles in disease development, but other HSTs are relatively minor. The HSTs identified to date are relatively small proteins, which can generate necrotic cell death in sensitive lines within 24 to 48 h whereas no necrosis is visible in insensitive lines. Each of these HSTs interact with host genes in an inverse gene-for-gene manner. In this scenario, individual HSTs interact directly or indirectly with a dominant host gene product to induce disease. Purification of the HST proteins and cloning of the genes responsible for HST production will be discussed.