A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens

Plant disease resistance is often conferred by genes with nucleotide binding site (NBS) and leucine-rich repeat (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...

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Main Authors: Faris, J., Zhang, Z., Lu, H., Lu, S., Reddy, L., Cloutier, S., Fellers, J., Meinhardt, S., Rasmussen, J., Xu, S., Oliver, Richard, Simons, K., Friesen, T.
Format: Journal Article
Published: National Academy of Sciences 2010
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Online Access:http://hdl.handle.net/20.500.11937/12471
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author Faris, J.
Zhang, Z.
Lu, H.
Lu, S.
Reddy, L.
Cloutier, S.
Fellers, J.
Meinhardt, S.
Rasmussen, J.
Xu, S.
Oliver, Richard
Simons, K.
Friesen, T.
author_facet Faris, J.
Zhang, Z.
Lu, H.
Lu, S.
Reddy, L.
Cloutier, S.
Fellers, J.
Meinhardt, S.
Rasmussen, J.
Xu, S.
Oliver, Richard
Simons, K.
Friesen, T.
author_sort Faris, J.
building Curtin Institutional Repository
collection Online Access
description Plant disease resistance is often conferred by genes with nucleotide binding site (NBS) and leucine-rich repeat (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 on wheat produce 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 have disease resistance gene-like features, including S/TPK and NBS-LRR domains. Mutagenesis revealed that all three domains are required for ToxA sensitivity, and hence disease susceptibility. 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 gene-fusion event that gave rise to its unique structure. Although Tsn1 is necessary to mediate ToxA recognition, yeast two-hybrid experiments suggested 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 may thrive by subverting the resistance mechanisms acquired by plants to combat other pathogens.
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publishDate 2010
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spelling curtin-20.500.11937-124712017-09-13T14:56:52Z A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens Faris, J. Zhang, Z. Lu, H. Lu, S. Reddy, L. Cloutier, S. Fellers, J. Meinhardt, S. Rasmussen, J. Xu, S. Oliver, Richard Simons, K. Friesen, T. map-based cloning disease resistance host–pathogen interaction Triticum necrotrophic fungus Plant disease resistance is often conferred by genes with nucleotide binding site (NBS) and leucine-rich repeat (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 on wheat produce 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 have disease resistance gene-like features, including S/TPK and NBS-LRR domains. Mutagenesis revealed that all three domains are required for ToxA sensitivity, and hence disease susceptibility. 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 gene-fusion event that gave rise to its unique structure. Although Tsn1 is necessary to mediate ToxA recognition, yeast two-hybrid experiments suggested 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 may thrive by subverting the resistance mechanisms acquired by plants to combat other pathogens. 2010 Journal Article http://hdl.handle.net/20.500.11937/12471 10.1073/pnas.1004090107 National Academy of Sciences fulltext
spellingShingle map-based cloning
disease resistance
host–pathogen interaction
Triticum
necrotrophic fungus
Faris, J.
Zhang, Z.
Lu, H.
Lu, S.
Reddy, L.
Cloutier, S.
Fellers, J.
Meinhardt, S.
Rasmussen, J.
Xu, S.
Oliver, Richard
Simons, K.
Friesen, T.
A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
title A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
title_full A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
title_fullStr A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
title_full_unstemmed A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
title_short A unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
title_sort unique wheat disease resistance-like gene governs effector-triggered susceptibility to necrotrophic pathogens
topic map-based cloning
disease resistance
host–pathogen interaction
Triticum
necrotrophic fungus
url http://hdl.handle.net/20.500.11937/12471