|Zhang, Zengcui -|
|Lu, Huangjun -|
|Cloutier, Sylvie -|
|Meinhardt, Steven -|
|Rasmussen, Jack -|
|Oliver, Richard -|
Submitted to: Proceedings of the National Academy of Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 18, 2010
Publication Date: July 27, 2010
Citation: Faris, J.D., Zhang, Z., Lu, H., Lu, S., Cloutier, S., Fellers, J.P., Meinhardt, S.W., Rasmussen, J.B., Xu, S.S., Oliver, R.P., Simons, K.J., Friesen, T.L. 2010. A Unique Wheat Disease Resistance-like Gene Governs Effector-Induced Susceptibility to Necrotrophic pathogens. Proceedings of the National Academy of Sciences. 107:13544-13549. Interpretive Summary: Plant disease resistance is often conferred by genes with specific features known as nucleotide binding and leucine-rich repeat(NB-LRR) or protein kinase (PK) domains. Here, we isolated the wheat gene Tsn1, which governs sensitivity to a host-selective toxin (ToxA) produced by two wheat necrotrophic pathogens that cause Stagonospora nodorum blotch and tan spot. Tsn1 has features of disease resistance genes, harboring PK and NB-LRR domains, all of which are required for ToxA sensitivity, and hence disease susceptibility. Tsn1 is unique to ToxA-sensitive wheat lines, and modern wheat acquired Tsn1 from a wild wheat ancestor through evolution.The Tsn1 protein does not interact directly with ToxA, and Tsn1 transcription is regulated by the circadian clock and light. This work provides strong evidence that necrotrophic pathogens thrive by subverting the resistance mechanisms acquired by plants to combat other pathogens.
Technical Abstract: Plant disease resistance is often conferred by genes with nucleotide binding site and leucine-rich repeat NBS-LRR) or serine/threonine protein kinase (S/TPK) domains. Much less is known about mechanisms of susceptibility, particularly to necrotrophic fungal pathogens. The pathogens that cause the diseases tan spot and Stagonospora nodorum blotch (SNB) on wheat produce virulence effectors (host-selective toxins) that induce susceptibility in wheat lines harboring corresponding toxin sensitivity genes. The effector ToxA is produced by both pathogens, and sensitivity to ToxA is governed by the Tsn1 gene on wheat chromosome arm 5BL. Here, we report the cloning of Tsn1, which was found to obtain features of disease resistance genes, including S/TPK and NBS-LRR domains.Mutagenesis revealed that all three domains are required for ToxA sensitivity, and hence disease susceptibility. Genotyping and Southern analysis indicated that Tsn1 is unique to ToxA-sensitive genotypes and insensitive genotypes are null. Sequencing and phylogenetic analysis indicated that Tsn1 arose in the B-genome diploid progenitor of polyploid wheat through a genome shuffling event that gave rise to its unique structure. Functional analysis indicated that the Tsn1 protein does not interact directly with ToxA. Tsn1 transcription is tightly regulated by the circadian clock and light, providing further evidence that Tsn1-ToxA interactions are associated with photosynthesis pathways. This work suggests that these necrotrophic pathogens thrive by subverting the resistance mechanisms acquired by plants to combat other pathogens.