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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Research » Research » Publications at this Location » Publication #137060
Title: GENETICS OF RESISTANCE TO TAN SPOT IN A RECOMBINANT INBRED POPULATION OF WHEAT.

Author
item FRIESEN, TIMOTHY - 5442-05-25
item KIANIAN, SHAHYAR - PLNT SCI, NDSU, FARGO, ND
item FRANCL, LEONARD - PLNT PATH NDSU, FARGO, ND
item RASMUSSEN, JACK - PLNT PATH NDSU, FARGO, ND

Submitted to: Tan Spot International Workshop Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 7/21/2002
Publication Date: 9/1/2003
Citation: Friesen, T.L., Kianian, S.F., Francl, L.J., Rasmussen, J.B. 2003. GENETICS OF RESISTANCE TO TAN SPOT IN A RECOMBINANT INBRED POPULATION OF WHEAT. Tan Spot International Workshop Proceedings. pg 103-107

Interpretive Summary:

Technical Abstract: The most efficient long-term approach to control tan spot of wheat, caused by Pyrenophora tritici-repentis, is through genetic resistance in the host. The hard red spring wheat cv. "Erik", both insensitive to Ptr ToxA and resistant to the fungus, has long been recognized as a potential source of tan spot resistance. The objective of this work was to identify genetic components of resistance in a population of 108 recombinant inbred lines derived from a cross between the toxin-sensitive and tan spot-susceptible cv. `Kulm' and Erik. As expected, the population segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the tan spot fungus; only 8 susceptible lines were identified. There were no transgressive segregants for either resistance or susceptibility. The host reaction to Ptr ToxA accounted for only 24.2% of the genetic variance associated with reaction to race 2. This suggests that toxin reaction is only a minor component of disease development. Bulked segregant analysis and microsatellite markers were used to identify a new quantitative trait locus (QTL) for resistance to tan spot. This locus, located on chromosome 6B, accounted for 8.8 % of the total phenotypic variance and for 12.3% of the genetic variance for disease. This locus and the host reaction to Ptr ToxA together accounted for 37.7% of the genetic variation for the disease phenotype. As many as five resistance genes, presumably all derived from Erik, may segregate in this population.