Author
|
Submitted to: Canadian Journal of Plant Pathology
Publication Type: Proceedings Publication Acceptance Date: 12/21/2009 Publication Date: 3/1/2010 Citation: Friesen, T.L., Faris, J.D. 2010. Characterization Of The Wheat-Stagonospora nodorum Disease System - What Is The Molecular Basis of This Quantitative Necrotrophic Disease Interaction. Canadian Journal of Plant Pathology 32:20-28 Interpretive Summary: Stagonospora nodorum blotch (SNB) of wheat is a major problem in wheat production areas throughout the world. This disease caused by the fungus Stagonospora nodorum affects both the leaves and glumes of susceptible bread and durum wheat. Resistance to both disease phases has been shown to be complexly inherited and although much effort has gone into the identification and introgression of disease resistance, less than satisfactory progress has been made in producing cultivars resistant to this disease. A major pitfall in this process has been the lack of understanding of the underlying mechanism of disease resistance. Recently, we have shown the Stagonospora nodorum–wheat interaction to involve toxins that interact with dominant wheat sensitivity/susceptibility gene products to induce disease. To date, we have reported five toxin–host gene interactions. In each case, toxin sensitivity and susceptibility is controlled by a single dominant gene and in all but one case the interaction is dependent on light. The toxin-host gene interactions have been shown to account for 18-95 percent of the disease variation, highlighting the importance of these interactions. Several unpublished interactions also exist making this a model system for studying necrotrophic diseases of plants. Technical Abstract: Stagonospora nodorum blotch (SNB) has long been a problem in wheat production areas by affecting both the leaves and glumes of susceptible bread and durum wheat. Resistance to both disease phases has been shown to be complexly inherited and although much effort has gone into the identification and introgression of disease resistance, less than satisfactory progress has been made in producing SNB resistant cultivars. A major pitfall in this process has been the lack of understanding of the underlying mechanism of disease resistance. Recently, we have shown the Stagonospora nodorum–wheat interaction to involve multiple effector proteins also known as host-selective toxins (HSTs) that interact either directly or indirectly with dominant wheat sensitivity/susceptibility gene products to induce disease. Therefore we have referred to this system as an “inverse gene-for-gene” interaction (i.e. effector triggered susceptibility) because the recognition of an effector protein by the host leads to susceptibility rather than resistance as it does in classical gene-for-gene interactions currently referred to as effector triggered immunity. To date, we have reported five HST–host gene interactions. In each case, toxin sensitivity and susceptibility is controlled by a single dominant gene and in all but one case the interaction is dependent on light. Using quantitative trait loci analysis, the toxin-host gene interactions have been shown to account for 18%-95% of the disease variation, highlighting the importance of these interactions. Several unpublished interactions also exist making this a model system for the investigation of the molecular mechanism of necrotrophic disease. |
