9:00 am - 10:00 am
A graduate exam seminar is a presentation of the student’s final research project for their degree.
This is an ALES MSc Final Exam Seminar by Bohan Wei. This seminar is open to the general public to attend.
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Meeting ID: 878 2471 6172
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Thesis Topic: Virulence of Pyrenophora tritici-repentis (Ptr) in relation to host type
MSc with Dr. Steve Strelkov.
Tan spot is a destructive foliar disease of wheat caused by the fungus Pyrenophora tritici-repentis (Ptr). Eight races (R1 to R8) of Ptr have been identified globally, based on their ability to produce different combinations of three necrotrophic effectors (NE): ToxA, ToxB and ToxC. ToxA causes necrosis, and ToxB and ToxC both induce chlorosis. The fungus was first identified from Agropyron repens, a common grass species in North America. While Ptr is known primarily as a pathogen of wheat, ToxB-producing isolates cause mild chlorosis on susceptible barley. In this thesis, Ptr race structure was investigated in relation to its different hosts. One hundred forty-four isolates of the fungus from durum, winter bread wheat, and grasses in western Canada were collected and evaluated for race classification on a host differential set, followed by PCR analysis for ToxA and ToxB to confirm race identity. The susceptibility of 114 durum (Canadian) and winter bread wheat (Canadian and European) genotypes to R2, R3, and R5, each producing one effector, was evaluated in bioassays, and the genetics of the Ptr-barley interaction were investigated for the first time. A doubled-haploid (DH) barley population was screened with R5 (ToxB) and 381 SNP markers were used to map the locus conditioning chlorosis. Ptr race composition varied based on the host from which the isolates were recovered. Races 1 and 2 were predominant on wheat and found with equal frequency on durum, while R1 occurred twice as frequently as R2 on winter wheat. Race 3 was recovered only from durum wheat, at a frequency of 8%; the non-pathogenic R4 was the only race recovered from grasses. Susceptibility to R2 (ToxA) and R3 (ToxC), the predominant races in Canada, was more common in Canadian bread and durum wheat than in European wheat. However, susceptibility to R5 (ToxB) was more common in durum and European winter wheat than in Canadian winter wheat. R5 is a dominant race on durum in regions encompassing the wheat centre of origin. Tsn1, the gene conferring sensitivity to ToxA, amplified at a higher percentage in Canadian (51.2% in winter bread, 59% in durum) vs. European (21.7%) wheat genotypes. The presence of Tsn1, however, did not result in susceptibility to ToxA-producing isolates in 10.7% and 35.9% of the Tsn1-coding winter and durum genotypes, respectively. This indicates, especially in durum, that ToxA-Tsn1 may not play a significant role in tetraploid wheat. Moreover, R3 and R5 caused necrosis, rather than chlorosis, on a number of genotypes, suggesting that these genotypes carry multiple alleles of the genes conferring sensitivity to ToxC and ToxB, and hence react more strongly, or that these races produce additional necrosis-inducing effectors. Susceptibility to Ptr in barley was dominantly inherited and controlled by a single locus designated here as Spr1, mapping to the distal region of the short arm of chromosome 2H. An understanding of host-pathogen relations in Ptr on its various hosts will aid in the enhanced management of this important pathogen.