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ARS Home » Plains Area » Manhattan, Kansas » Center for Grain and Animal Health Research » Hard Winter Wheat Genetics Research » Research » Publications at this Location » Publication #357916

Research Project: Genetic Improvement of Biotic and Abiotic Stress Tolerance and Nutritional Quality in Hard Winter Wheat

Location: Hard Winter Wheat Genetics Research

Title: Identification of quantitative trait loci conferring resistance to tan spot in a biparental population derived from two Nebraska hard red winter wheat cultivars

item KARIYAWASAM, GAYAN - North Dakota State University
item HUSSAIN, WASEEM - University Of Nebraska
item EASTERLY, AMANDA - University Of Nebraska
item Guttieri, Mary
item BELAMKAR, VIKAS - University Of Nebraska
item POLAND, JESSE - Kansas State University
item VENEGAS, JORGE - University Of Nebraska
item BAENZIGER, P. STEPHEN - University Of Nebraska
item MARAIS, FRANCOIS - North Dakota State University
item RASMUSSEN, JACK - North Dakota State University
item LIU, ZHAOHUI - North Dakota State University

Submitted to: Molecular Breeding
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/30/2018
Publication Date: 11/14/2018
Citation: Kariyawasam, G.K., Hussain, W., Easterly, A., Guttieri, M.J., Belamkar, V., Poland, J., Venegas, J., Baenziger, P., Marais, F., Rasmussen, J.B., Liu, Z. 2018. Identification of quantitative trait loci conferring resistance to tan spot in a biparental population derived from two Nebraska hard red winter wheat cultivars. Molecular Breeding. 38:140.

Interpretive Summary: Tan spot is a destructive disease that affects the foliage of wheat. Wheats resistant to tan spot are the preferred tool for reducing yield and quality losses due to this disease. The winter wheat variety Wesley is known to be highly resistant, but the genetic control of this resistance has not been well characterized, which limits its use in modern wheat breeding programs. This research used a segregating population from a cross between a susceptible wheat variety, Harry, and the resistant variety, Wesley, to identify regions of the wheat genome associated with tan spot resistance. We concluded that Wesley lacks both the susceptibility conferred by the known Tsn1 gene on chromosome 5B and likely lacks the susceptibility conferred by the known Tsc1 locus on chromosome 1A. Three additional regions of the genome, on 7A, 7B, and 7D appear to have minor effects on tan spot sensitivity. These results will help breeders use the complex resistance in Wesley to effectively breed for resistance to tan spot.

Technical Abstract: Tan spot, caused by Pyrenophora tritici-repentis (Ptr), is a destructive foliar disease in all types of cultivated wheat worldwide. Genetics of tan spot resistance in wheat is complex, involving insensitivity to fungal-produced necrotrophic effectors (NEs), major resistance genes and quantitative trait loci (QTL) conferring race-nonspecific and racespecific resistance. The Nebraska hard red winter wheat (HRWW) cultivar 'Wesley' is insensitive to Ptr ToxA and highly resistant to multiple Ptr races, but the genetics of resistance in this cultivar is unknown. In this study, we used a recombinant inbred line (RIL) population derived from a cross between Wesley and another Nebraska cultivar 'Harry' (Ptr ToxA sensitive and highly susceptible) to identify QTL associated with reaction to tan spot caused by multiple races/isolates. Sensitivity to Ptr ToxA conferred by the Tsn1 gene was mapped to chromosome 5B as expected. The Tsn1 locus was a major susceptibility QTL for the race 1 and race 2 isolates, but not for the race 2 isolate with the ToxA gene deleted. A second major susceptibility QTL was identified for all the Ptr ToxC-producing isolates and located to the distal end of the chromosome 1A, which likely corresponds to the Tsc1 locus. Three additional QTL with minor effects were identified on chromosomes 7A, 7B and 7D. This work indicates that both Ptr ToxATsn1 and Ptr ToxC-Tsc1 interactions are important for tan spot development in winter wheat, and Wesley is highly resistant largely due to the absence of the two tan spot sensitivity genes.