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Studies on the Role and Mechanism of Action of Ptr ToxB from Pyrenophora tritici-repentis

Posted on:2013-12-11Degree:Ph.DType:Thesis
University:University of Alberta (Canada)Candidate:Kim, Yong MinFull Text:PDF
GTID:2453390008970005Subject:Agriculture
Abstract/Summary:
Tan spot is an important foliar disease of wheat caused by Pyrenophora tritici-repentis. This fungus produces Ptr ToxB, a host-specific toxin that induces chlorosis on sensitive host genotypes. An assessment of the effects of Ptr ToxB in a toxin-sensitive wheat line revealed that photosynthesis, as measured by infra-red gas analysis, declined significantly prior to the development of chlorosis. This decline was accompanied by changes in the leaf proteome, with 102 protein spots found to have altered intensities by 2-dimensional gel electrophoresis 12-36 h after toxin treatment. Forty-seven of these spots were identified by tandem mass spectrometry and included proteins involved in the light reactions of photosynthesis, the Calvin cycle, and the stress/defense response. These results suggest that Ptr ToxB disrupts photosynthesis in sensitive wheat, leading to oxidative stress and chlorophyll photooxidation. In another study, the ToxB gene encoding Ptr ToxB was transformed into a Ptr ToxB-non-producing isolate of P. tritici-repentis. The transformants induced chlorosis in a host-specific manner and caused significantly increased disease, with symptom severity correlated with the amount of Ptr ToxB produced. These findings indicate that the acquisition of toxin-producing ability is a sufficient condition for pathogenicity in P. tritici-repentis, and that Ptr ToxB confers virulence in a dosage-dependent manner. In a final study to explore the possible role(s) of ToxB homologs found in other ascomycetes, Pyrenophora teres, which causes net blotch of barley, was transformed with ToxB. Production of Ptr ToxB by P. teres increased virulence on net blotch-resistant and susceptible barley cultivars. However, while the transformants exhibited an altered infection phenotype on toxin-sensitive wheat, they did not cause the typical chlorosis associated with tan spot. This suggests that while ToxB homologs may play a role in the pathogenicity of this fungus, production of Ptr ToxB is on its own not sufficient for P. teres virulence on wheat. Collectively, these studies improved understanding of the role of Ptr ToxB in tan spot development and fungal virulence. An enhanced knowledge of tan spot and related pathosystems will facilitate rational strategies for disease management.
Keywords/Search Tags:Ptr toxb, Tan spot, Tritici-repentis, Pyrenophora, Role, Disease, Wheat, Virulence
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