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K-State Today

November 20, 2014

Lecture today about induction, exploitation of plant cell suicide

Submitted by Stephanie Alvord-Albanese

Zhaohui Liu, assistant professor in plant pathology at North Dakota State University, will present "Induction and exploitation of plant cell suicide: How Parastagonospora nodorum causes disease" from 3:45–4:45 p.m. Nov. 20, in 4031 Throckmorton Hall.

The lecture abstract:
The fungus Parastagonospora nodorum (synonym: Stagonospora nodorum, Septoria nodorum) is the causal agent of Stagonospora nodorum leaf and glume blotch (SNB), an economically important wheat disease in many wheat-growing areas around the world. The disease system was previously known as being lack of clear gene-for-gene relationship and presence of quantitatively inherited resistance. In the past decade, however, a substantial progress has been made in understanding the genetic and molecular basis of SNB based on our research work and others. It has been revealed that the fungus produces multiple necrotrophic effectors (NEs), also known as host-selective toxins, to induce necrosis and promote disease by interacting with their corresponding host sensitivity genes. Currently, seven pairs of NE-host sensitivity gene interactions have been characterized in the SNB system, including SnToxA-Tsn1, SnTox1-Snn1, SnTox2-Snn2, SnTox3-Snn3-B1, SnTox3-Snn3-D1, SnTox4-Snn4, and SnTox5-Snn5. Because the effect of each interaction on disease is additive, resistance/susceptibility is often observed as a quantitative trait. All identified P. nodorum NEs are small proteins, and the fungal genes encoding for SnToxA, SnTox1 and SnTox3 have been isolated. The SnToxA-encoding gene (SnToxA) is nearly identical to the ToxA gene that was first cloned from Pyrenophora tritici-repentis, the fungus causing wheat tan spot. Strong evidence suggested that ToxA was originally present in P. nodorum, and later acquired by P. tritici-repentis through a horizontal gene transfer. SnTox1 and SnTox3 are cysteine-rich proteins, but have no significant similarity to any other proteins in the NCBI database. SnTox1 was shown to induce defense gene expression, oxidative burst, and DNA laddering in plant, all of which are hallmarks of resistance. This provided further evidence that P. nodorum, as a necrotrophic fungal pathogen, utilizes these NEs to induce and exploit plant resistance mechanism (programmed cell death) for colonization. SnTox1 has a predicted chitin-binding domain and the SnTox1-encoding gene is present in the majority of P. nodorum isolates collected from diverse geographic locations. We speculated that in addition to necrosis-inducing activity, SnTox1 has a protection function for the fungus comparable to Avr4 in tomato-Cladosporium fulvum system. The presentation will provide an overview on our current understanding of the SNB system at the molecular level and focus on our recent studies on the mode of action of SnTox1.