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United States Department of Agriculture

Agricultural Research Service

Title: Role of Host Sensitivity to Ptr Toxa in Development of Tan Spot of Wheat.

Authors
item Friesen, Timothy
item Ali, S. - PLNT PATH NDSU, FARGO, ND
item Kianian, S. - PLNT SCI, NDSU, FARGO, ND
item Francl, L. - PLNT PATH NDSU, FARGO, ND
item Rasmussen, J. - PLNT PATH NDSU, FARGO, ND

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 15, 2002
Publication Date: April 1, 2003
Citation: FRIESEN, T.L., ALI, S., KIANIAN, S., FRANCL, L.J., RASMUSSEN, J.B. ROLE OF HOST SENSITIVITY TO PTR TOXA IN DEVELOPMENT OF TAN SPOT OF WHEAT.. PHYTOPATHOLOGY. 2003. V. 93(4). p. 397-401.

Interpretive Summary: The objective of this research was to evaluate the role of host sensitivity to Ptr ToxA, a host selective toxin produced by the tan spot causing fungus Pyrenophora tritici-repentis, in the disease development by P. tritici-repentis race 2. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritibility estimates suggested the presence of 4 to 5 genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived from Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.

Technical Abstract: Pyrenophora tritici-repentis race 2 produces Ptr ToxA, a host-selective toxin previously described as a pathogenicity factor for tan spot on wheat. The objective of this research was to evaluate the role of host sensitivity to toxin, conditioned by a single dominant gene on chromosome 5BL, in the disease development by race 2. An F2-derived F6 recombinant inbred population of 108 wheat lines, produced from crosses of toxin-sensitive, disease-susceptible cv. 'Kulm' with the toxin-insensitive, disease-resistant cv. 'Erik', segregated 1:1 for toxin reaction. However, the population was skewed toward resistance to race 2 of the fungus. Toxin reaction accounted for 24.4% of the genetic variance for disease. Heritibility estimates suggested the presence of 4 to 5 genes that influence disease reaction in the population. Toxin-insensitive mutants, previously derived Kulm, were susceptible to race 2, although disease developed more slowly on the mutants than it did on the wild type Kulm. The data indicate that sensitivity to Ptr ToxA influences disease severity in some host genotypes without defining susceptibility.

Last Modified: 4/19/2014
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