Tan spot susceptibility governed by the Tsn1 locus and race-nonspecific resistance quantitative trait loci in a population derived from the wheat lines Salamouni and Katepwa

Abstract

Wheat–tan spot interactions are known to have an inverse gene-for-gene relationship where pathogen-produced necrotrophic effectors are recognized by host sensitivity genes to cause susceptibility. However, broad-spectrum race-nonspecific resistance quantitative trait loci (QTL) that do not conform to the inverse gene-for-gene model have also been identified in this system. Here, we evaluated a population of wheat recombinant inbred lines derived from Salamouni (resistant) and Katepwa (susceptible) for reaction to two isolates of race 1 (Pti2 and Asc1) and one isolate of race 2 (86–124), which all produce the necrotrophic effector Ptr ToxA, and the isolate AR LonB2, which does not produce Ptr ToxA and does not conform to the current race classification system. As expected, the Tsn1 locus was significantly associated with disease caused by all three ToxA-producing isolates and was not associated with tan spot caused by AR LonB2. However, the amount of variation explained by Tsn1 varied considerably, with values of 5, 22, and 30 % for Asc1, Pti2, and 86–124, respectively, suggesting possible variability in ToxA gene regulation among these isolates. A locus on chromosome arm 7DS was specifically associated with isolate AR LonB2 but explained only 8 % of the variation. Additional QTL on 5DL and 7BS were race-nonspecific and associated with tan spot caused by multiple isolates. These results provide further evidence that race-nonspecific resistance QTL play important roles in governing reaction to tan spot, and they suggest that the wheat–tan spot pathosystem is more complicated than previously thought. The elimination of necrotrophic effector sensitivity genes and the addition of race-nonspecific resistance loci are needed to develop wheat cultivars with high levels of tan spot resistance.