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Arabidopsis TAO1 is a TIR-NB-LRR protein that contributes to disease resistance induced by the Pseudomonas syringae effector AvrB

Eitas, Timothy K. and Nimchuk, Zachary L. and Dangl, Jeffrey L. (2008) Arabidopsis TAO1 is a TIR-NB-LRR protein that contributes to disease resistance induced by the Pseudomonas syringae effector AvrB. Proceedings of the National Academy of Sciences of the United States of America, 105 (17). pp. 6475-6480. ISSN 0027-8424. http://resolver.caltech.edu/CaltechAUTHORS:EITpnas08

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Abstract

The type III effector protein encoded by avirulence gene B (AvrB) is delivered into plant cells by pathogenic strains of Pseudomonas syringae. There, it localizes to the plasma membrane and triggers immunity mediated by the Arabidopsis coiled-coil (CC)-nucleotide binding (NB)-leucine-rich repeat (LRR) disease resistance protein RPM1. The sequence unrelated type III effector avirulence protein encoded by avirulence gene Rpm1 (AvrRpm1) also activates RPM1. AvrB contributes to virulence after delivery from P. syringae in leaves of susceptible soybean plants, and AvrRpm1 does the same in Arabidopsis rpm1 plants. Conditional overexpression of AvrB in rpm1 plants results in leaf chlorosis. In a genetic screen for mutants that lack AvrB-dependent chlorosis in an rpm1 background, we isolated TAO1 (target of AvrB operation), which encodes a Toll-IL-1 receptor (TIR)-NB-LRR disease resistance protein. In rpm1 plants, TAO1 function results in the expression of the pathogenesis-related protein 1 (PR-1) gene, suggestive of a defense response. In RPM1 plants, TAO1 contributes to disease resistance in response to Pto (P. syringae pathovars tomato) DC3000(avrB), but not against Pto DC3000(avrRpm1). The tao1–5 mutant allele, a stop mutation in the LRR domain of TAO1, posttranscriptionally suppresses RPM1 accumulation. These data provide evidence of genetically separable disease resistance responses to AvrB and AvrRpm1 in Arabidopsis. AvrB activates both RPM1, a CC-NB-LRR protein, and TAO1, a TIR-NB-LRR protein. These NB-LRR proteins then act additively to generate a full disease resistance response to P. syringae expressing this type III effector.


Item Type:Article
Additional Information:© 2008 by The National Academy of Sciences of the USA. Contributed by Jeffery L. Dangl, March 4, 2008 (received for review August 12, 2007). Freely available online through the PNAS open access option. We thank Drs. David Mackey, Ai-Jiuan Wu, and Marc Nishimura for critical reading of the manuscript, and Dr. David A. Hubert and Dr. Petra Epple for technical suggestions. This work was supported by Department of Energy Grant DE-FG05-95ER20187 (to J.L.D.). Author contributions: T.K.E. and Z.L.N. contributed equally to this work; T.K.E., Z.L.N., and J.L.D. designed research; T.K.E. and Z.L.N. performed research; T.K.E., Z.L.N., and J.L.D. analyzed data; and T.K.E., Z.L.N., and J.L.D. wrote the paper. The authors declare no conflict of interest. Data deposition: The sequences reported in this paper have been deposited in the GenBank database (accession nos. EU031442 and EU031443). This article contains supporting information online at www.pnas.org/cgi/content/full/0802157105/DCSupplemental.
Issue or Number:17
Record Number:CaltechAUTHORS:EITpnas08
Persistent URL:http://resolver.caltech.edu/CaltechAUTHORS:EITpnas08
Alternative URL:http://dx.doi.org/10.1073/pnas.0802157105
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:10334
Collection:CaltechAUTHORS
Deposited By: Archive Administrator
Deposited On:30 Apr 2008
Last Modified:14 Nov 2014 19:20

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