Botany and Plant Pathology Seminar Series
Speaker: Dr. Tim Friesen - Department of Plant Pathology - North Dakota State University
Topic: Stagonospora nodorum blotch on wheat; exposing the arsenal of a necrotrophic pathogen
When: Wednesday, September 19, 2012 at 3:30 pm in WSLR 116
Abstract:

Several fungal plant pathogens in the Dothideomycete class produce necrotrophic effectors (synonym: host selective toxins) that induce susceptibility. Mounting evidence indicates that recognition of these necrotrophic effectors is often governed by host genes with resistance gene-like signatures including both nucleotide binding (NB) and leucine rich repeat (LRR) domains. Necrotrophic pathogens often use a mechanism whereby effectors are secreted into the host environment to elicit programmed cell death (PCD) but rather than inhibiting the pathogen, the necrotrophic pathogen benefits from PCD by gaining nutrient from the dying cells. This is in contrast to the classical effector triggered immunity (ETI) model where effector recognition followed by R-gene signaling results in the inhibition of pathogen growth. The Stagonospora nodorum-wheat interaction is a classic example of a necrotrophic interaction. Our research on the S. nodorum-wheat interaction indicates that the pathogen secretes as many as twenty necrotrophic effectors that interact specifically with host gene products to modulate host defense mechanisms to its advantage. Most recently we have characterized the SnTox1-Snn1 interaction and have demonstrated that this effector-host gene interaction shows hallmarks of PCD including up regulation of defense response genes, induction of an early oxidative burst, and DNA laddering but the end result is susceptibility rather than resistance. Additionally, SnTox1 has some striking similarities to proteins involved in chitin binding, indicating that SnTox1 may have a dual role in pathogenesis. This research provides important insights into the molecular basis of the wheat-S. nodorum interaction, an emerging model for necrotrophic pathosystems.

 

 

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