1a.Objectives (from AD-416):
The objectives of this cooperative research project are: . 1)identify tan spot and Stagonospora nodorum blotch resistance genes in wheat,. 2)determine the chromosomal locations of the resistance genes, and. 3)identify or develop markers suitable for marker-assisted selection of the resistance genes.
1b.Approach (from AD-416):
A recombinant inbred (RI) population derived from a cross between the resistant wheat landrace Salamouni and the susceptible Canadian variety Katepwa will be developed for the identification and mapping of novel resistance genes. The RI population will be genotyped with molecular markers, and linkage maps representing all 21 wheat chromosomes will be assembled. The population of RI lines will be screened for reaction to multiple races of the tan spot fungus and isolates of S. nodorum. The phenotypic data will be regressed on the molecular marker data to identify quantitative trait loci (QTL) associated with resistance. Genomic regions harboring significant QTL will be targeted for saturation mapping to identify and/or develop user-friendly PCR-based markers tightly linked to the QTL for marker-assisted selection.
The experimental population derived from the wheat lines Salamouni and Katepwa was genotyped with 484 molecular markers. The marker data was used to assemble genetic linkage maps of all 21 wheat chromosomes. The entire population was also screened for reaction to the S. nodorum host-selective toxins SnToxA, SnTox1, SnTox3, and SnTox4. Reactions to these toxins provided the data necessary for mapping the genes that recognize these toxins and lead to disease susceptibility, i.e. Tsn1, Snn1, Snn3, and Snn4, respectively. The entire population was also screened for reaction to disease caused by the S. nodorum isolate Sn99CH 1A7A, which produces the host-selective toxin SnTox4. The phenotypic data was analyzed in conjunction with the genotypic data and genetic linkage maps to identify regions of the wheat chromosomes (quantitative trait loci) that harbored genes governing resistance or susceptibility to isolate Sn99CH 1A7A and to evaluate the effects of the Snn4-SnTox4 interaction in causing disease. The results indicated that interaction between the wheat gene Snn4 and the pathogen-produced host-selective toxin SnTox4 accounted for 23.5% of the variation in disease. In addition to this, a gene on wheat chromosome 7A was significantly associated with disease resistance and accounted for 16.5% of the variation. Therefore, objectives 1 and 2, as they related to the wheat disease Stagonospora nodorum blotch, were accomplished.