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Virulence of Pyrenophora tritici-repentis in relation to host type

  • Author / Creator
    Wei, Bohan
  • Tan spot is a destructive foliar disease of wheat caused by the fungus Pyrenophora tritici-repentis (Ptr). Eight races (race 1 to race 8) of Ptr have been identified globally, based on their ability to produce different combinations of three necrotrophic effectors (NE): Ptr ToxA, Ptr ToxB, and Ptr ToxC. Ptr ToxA causes necrosis, and Ptr ToxB and Ptr 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, Ptr 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 race 2, race 3, and race 5, 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 race 5 (Ptr 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 race 1 occurred twice as frequently as race 2 on winter wheat. Race 3 was recovered only from durum wheat, at a frequency of 8%; the non-pathogenic race 4 was the only race recovered from grasses. Susceptibility to race 2 (Ptr ToxA) and race 3 (Ptr ToxC), the predominant races in Canada, was more common in Canadian bread and durum wheat than in European wheat. However, susceptibility to race 5 (Ptr ToxB) was more common in durum and European winter wheat than in Canadian winter wheat. Race 5 is a dominant race on durum in regions encompassing the wheat centre of origin. Tsn1, the gene conferring sensitivity to Ptr ToxA, amplified at a higher percentage in Canadian (51.2% in winter bread, 59% in durum) vs. European (20.5%) wheat genotypes. The presence of Tsn1, however, did not result in susceptibility to Ptr ToxA-producing isolates in 10.7% and 35.9% of the Tsn1-coding winter and durum genotypes, respectively. This indicates, especially in durum, that Ptr ToxA-Tsn1 may not play a significant role in tetraploid wheat. Moreover, races 3 and 5 caused necrosis, rather than chlorosis, on a number of genotypes, suggesting that these genotypes carry multiple alleles of the genes conferring sensitivity to Ptr ToxC and Ptr 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.

  • Subjects / Keywords
  • Graduation date
    Fall 2020
  • Type of Item
    Thesis
  • Degree
    Master of Science
  • DOI
    https://doi.org/10.7939/r3-qpgk-0730
  • License
    Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.