ARS | Publication request: Pathogen Exploitation of Gene-for-Gene Resistance Mechanisms in the Wheat-Stagonospora nodorum Pathosystem

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: November 12, 2009
Publication Date: January 9, 2010
Citation: Faris, J.D., Zhang, Z., Lu, S., Lu, H., Reddy, L., Cloutier, S., Fellers, J.P., Meinhardt, S.W., Rasmussen, J.B., Xu, S.S., Simons, K.J., Friesen, T.L. 2010. Pathogen Exploitation of Gene-for-Gene Resistance Mechanisms in the Wheat-Stagonospora nodorum Pathosystem. Meeting Abstract. pg.136

Technical Abstract: Stagonospora nodorum is a necrotrophic fungal pathogen of wheat that causes Stagonospora nodorum blotch (SNB). The wheat-S. nodorum pathosystem is a toxin-based system that relies on effector triggered susceptibility (ETS) to cause disease. This system is the mirror image of classical biotrophic pathogen –host interactions that involve recognition of a pathogen produced effector by a corresponding host resistance (R) gene, which leads to effector triggered immunity (ETI). To date, we have reported the identification of five host-toxin interactions in the wheat-S. nodorum pathosystem, all of which play important roles in conferring disease susceptibility. ToxA, which was recently involved in a lateral transfer from S. nodorum to the tan spot pathogen, was one of the first S. nodorum HSTs to be described. Sensitivity to ToxA is governed by the Tsn1 locus on wheat chromosome arm 5BL. Map-based cloning and validation by mutagenesis revealed that Tsn1 contains R gene-related protein kinase, nucleotide binding, and leucine-rich repeat domains, all of which are required for toxin sensitivity. Phylogenetic and comparative analysis of the Tsn1 locus with rice, Brachypodium, and the homoeologous region of wheat chromosome 5A indicates that Tsn1 arose relatively recently through domain shuffling. Tsn1 transcription is highly sensitive to light and is drastically reduced under dark conditions, which explains the fact that compatible Tsn1-ToxA interactions are light dependent. This work provides strong evidence for the notion that S. nodorum, and probably other necrotrophic pathogens, have acquired mechanisms to exploit biotrophic ETI mechanisms to cause disease.