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...
Saved in:
Published in: | Proceedings of the National Academy of Sciences - PNAS Vol. 107; no. 30; pp. 13544 - 13549 |
---|---|
Main Authors: | , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
National Academy of Sciences
27-07-2010
National Acad Sciences |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | 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. |
---|---|
Bibliography: | http://dx.doi.org/10.1073/pnas.1004090107 http://hdl.handle.net/10113/44178 2Present address: Texas Agrilife Research and Extension Center, Amarillo, TX 79106. 3Present address: Avesthagen Ltd., International Tech Park, Bangalore 560066, India. Edited by Steven P. Briggs, University of California of San Diego, La Jolla, CA, and approved June 17, 2010 (received for review March 26, 2010) Author contributions: J.D.F., Z.Z., H.L., and S.L. designed research; J.D.F., Z.Z., H.L., S.L., L.R., S.C., J.P.F., S.W.M., J.B.R., S.S.X., R.P.O., K.J.S., and T.L.F. performed research; J.D.F., Z.Z., H.L., and S.L. analyzed data; and J.D.F. and Z.Z. wrote the paper. |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.1004090107 |