Identifying resistance to tan spot disease in winter and durum wheat

Project Description

The proposed project aims to identify new sources of resistance to tan spot in durum and winter wheat.

Tan spot is a destructive foliar disease of wheat that can damage growing plants anytime during crop development causing millions of dollars in losses. Eight races (R1 to R8) of resistance to tan spot have been reported around the globe, but in Canada, USA and Australia two races (R1 and R2) are predominant. It affects nearly all common and durum wheat cultivars available to Canadian farmers and the lack of resistance to tan spot in winter and durum wheat is overlooked in most wheat breeding programs. The threat posed by new races to Canadian wheat is imminent, particularly with recent reports on emergence of novel strains in the USA, South America and North Africa.

Genetic resistance is the most cost effective and durable approach to manage tan spot. The objective of this project is to identify different tan spot resistance sources in durum and winter wheat, and to explore the pathogen variability in relation to specific wheat ploidy level or class. The proposed project will advance our knowledge with regards to tan spot resistance and variability on which durable resistance strategies can be advanced.

Research Results

Tan spot is one of the most destructive foliar wheat diseases in Canada. The causing pathogen is Pyrenophora tritici-repentis(Ptr),a fungus known to produce combinations of three effectors (toxins), namely ToxA, ToxB and ToxC. In Canada, ToxA is known as the most prevalent toxin and the only necrosis inducing factor.

In this project, the Ptr race structure on durum and winter bread wheat was investigated in Alberta and Saskatchewan. Previous research over the last 40 years has focused on spring bread wheat. The assumption in the proposal was that Ptr diversity may vary depending on the host type and the intensive survey from hexaploid (bread)wheat over the years may underestimated the presence of other races and toxins. In total, 144 Ptr single-spore isolates were recovered from durum, winter bread wheat, and grasses, and were evaluated for race identity on a wheat differential set, followed by PCR analysis for detecting the presence/absence of Ptr known effector (toxins) genes. Moreover, the susceptibility of 114 Canadian durum and winter wheat (Canadian and European) genotypes to races 2, 3, and 5 of Ptr, which produce the three known necrotrophic effectors ToxA, ToxB and ToxC, respectively, was evaluated in bioassays. Wheat lines were also tested for the presence of Tsn1, the dominant sensitivity gene for ToxA.

The results showed that race composition varied based on the host type from which the isolates were recovered; on durum, races 1 and 2 were present at a 1:1 ratio, while race 1 occurred twice as race 2 on winter bread wheat. Race 3 was recovered only from durum wheat, and the non-pathogenic race 4 was the only race to be collected from grasses. Susceptibility to race 2 was at least two-fold more common in Canadian winter wheat than in European genotypes and durum, while susceptibility to race 3 in Canadian winter bread and durum wheat occurred at an almost equal percentage and was twice higher than the susceptibility reported in European germplasm. Susceptibility to race 5 was more common in durum than in bread wheat. Tsn1 amplified at a higher percentage in Canadian wheat genotypes (51.2% in winter bread vs. 59% in durum) than in European (21.7%) genotypes. The presence of Tsn1 did not translate to susceptibility to ToxA-producing isolates in 10.7% and 35.9% of the winter bread and durum wheat genotypes carrying the Tsn1 gene, respectively. This indicates, especially in durum, that other factors are involved in the Ptr-durum interaction and that ToxA–Tsn1 may not play a significant role in durum wheat. Moreover, the chlorosis-inducing races 3 and 5 caused an atypical reaction, extensive necrosis, on a number of durum and winter wheat genotypes. This suggests that either: (1) these genotypes carry multiple alleles of Tsc1 and Tsc2, the genes conferring sensitivity to ToxC and ToxB, respectively, and hence react more strongly to races 3 and 5, or (2) these races produce additional necrosis causing effectors that await further identification.