1. The Salk Institute, La Jolla, California 92037, USA
2. John Innes Centre, Norwich NR4 7UH, UK
3. Department of Botany, University of Toronto, Ontario M5S 3B2, Canada
4. The Noble Foundation, Ardmore, Oklahoma 73401, USA
5. Present address: University of Edinburgh, Edinburgh EH9 3JR, UK.
6. These authors contributed equally to this work

Correspondence to: Robin K. Cameron^1,6,3 Correspondence and requests for materials should be addressed to R.K.C. (e-mail: Email: rcameron@botany.utoronto.ca). The Genbank accession number for DIR1 is AF342726.

Abstract

Localized attack by a necrotizing pathogen induces systemic acquired resistance (SAR) to subsequent attack by a broad range of normally virulent pathogens. Salicylic acid accumulation is required for activation of local defenses, such as pathogenesis-related protein accumulation, at the initial site of attack, and for subsequent expression of SAR upon secondary, distant challenge^{1, 2}. Although salicylic acid moves through the plant, it is apparently not an essential mobile signal². We screened Agrobacterium tumefaciens transfer DNA (tDNA) tagged lines of Arabidopsis thaliana for mutants specifically compromized in SAR. Here we show that Defective in induced resistance 1-1 (dir1-1) exhibits wild-type local resistance to avirulent and virulent Pseudomonas syringae, but that pathogenesis-related gene expression is abolished in uninoculated distant leaves and dir1-1 fails to develop SAR to virulent Pseudomonas or Peronospora parasitica. Petiole exudate experiments indicate that dir1-1 is defective in the production or transmission from the inoculated leaf of an essential mobile signal. DIR1 encodes a putative apoplastic lipid transfer protein and we propose that DIR1 interacts with a lipid-derived molecule to promote long distance signalling.