9:00 am - 10:00 am
3-18J Agricultural/Forestry Centre, University of Alberta, Edmonton AB
Event details: 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 Claudia Escobar Gil. This seminar is open to the general public to attend.
MSc with Drs. Stephen Strelkov and Leonardo Galindo Gonzalez.
Thesis Topic: Transcriptome analysis of the fungal pathogen Pyrenophora tritici-repentis, causal agent of tan spot of wheat
Tan spot, caused by the necrotrophic fungus Pyrenophora tritici-repentis, is a foliar disease of hexaploid and tetraploid wheat (Triticum aestivum and T. turgidum, respectively) that can cause significant yield and quality losses. Disease development involves the differential production of necrotrophic effectors (NEs) by races of P. tritici-repentis. Although three NEs, termed Ptr ToxA, Ptr ToxB, and Ptr ToxC, have been identified to date, the complete set of effectors and mechanisms contributing to fungal pathogenesis has yet to be fully elucidated. To improve understanding of the virulence of P. tritici-repentis, the fungal transcriptome was analyzed in planta by high-throughput RNA-sequencing (RNA-seq). The susceptible hexaploid wheat cultivar ‘Katepwa’ was inoculated with P. tritici-repentis isolates 86-124 (race 2, ToxA+) and Alg3-24 (race 5, ToxB+), and leaves were sampled at 12, 36 and 72 hours post-inoculation (hpi) to monitor changes in the pathogen transcriptome. Results were compared with the same isolates grown saprophytically in pure culture. RNA-seq analysis revealed some differences in the transcriptomes of Alg3-24 and 86-124, with the latter showing a higher number of upregulated genes related to the stress response. In general, however, the transcriptomic changes associated with infection were similar in both isolates, involving genes related to oxidative processes, fungal growth and plant cell wall degradation. These included genes coding for peroxidases, catalases and xylanases, which have been reported to enhance pathogenicity in other microbes. Both Alg3-24 and 86-124 presented more downregulated vs. upregulated genes. The ToxA gene coding for Ptr ToxA was expressed at 12 and 36 hpi, whereas the ToxB gene coding for Ptr ToxB showed a more uniform expression pattern across time points. Collectively, the results indicate significant changes in the transcriptome of P. tritici-repentis during pathogenesis and the involvement of various virulence-related processes beyond the known NEs.