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United States Department of Agriculture

Agricultural Research Service

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Research Project: Identification and Mapping of Disease Resistance Genes in Wheat

Location: Cereal Crops Research

2013 Annual Report


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.


3.Progress Report:

The RI population derived from the parental lines Salamouni and Katepwa was infiltrated with Ptr ToxA, a host-selective toxin produced by Pyrenophora tritici-repentis, which is the fungus that causes the disease tan spot. Each RI line was determined to be either sensitive or insensitive to the toxin, which allowed us to determine the chromosomal location of the Tsn1 gene in this population. The Tsn1 gene, which governs sensitivity to Ptr ToxA, mapped to the long arm of chromosome 5B. To determine the level of significance of Tsn1 in conferring tan spot disease, we inoculated the RI population with a fungal isolate known to produce Ptr ToxA. The results revealed that a compatible Tsn1-Ptr ToxA interaction explained as much as 30% of the variation in tan spot development in this population.


Last Modified: 10/21/2014
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