| Autor: |
Justin D. Faris, Zengcui Zhang, Huangjun Lu, Shunwen Lu, Reddy, Leela, Cloutier, Sylvie, Fellers, John P., Meinhardt, Steven W., Rasmussen, Jack B., Xu, Steven S., OIiver, Richard P., Simons, Kristin J., Friesen, Timothy L. |
| Předmět: |
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| Zdroj: |
Proceedings of the National Academy of Sciences of the United States of America; 7/27/2010, Vol. 107 Issue 30, p13544-13549, 6p |
| Abstrakt: |
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 Tsnl gene on wheat chromosome arm 5BL. Here, we report the cloning of Tsnl, which was found to have disease resistance gene-like features, including SITPK and NBS-LRR domains. Mutagenesis revealed that all three domains are required for ToxA sensitivity, and hence disease susceptibility. Tsnl is unique to ToxA-sensitive genotypes, and insensitive genotypes are null. Sequencing and phylogenetic analysis indicated that Tsnl arose in the B-genome diploid progenitor of polyploid wheat through a gene-fusion event that gave rise to its unique structure. Although Tsnl is necessary to mediate ToxA recognition, yeast two-hybrid experiments suggested that the Tsnl protein does not interact directly with ToxA. Tsn1 transcription is tightly regulated by the circadian clock and light, providing further evidence that Tsnl-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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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