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Summary Systemic acquired resistance (SAR) appears to be a ubiquitous higher plant defence response. Resistance is dependent on the high-level expression of SAR genes. Mutations, transgenes or chemicals that cause high-level SAR gene expression also cause resistance to pathogens. Furthermore, when SAR is eliminated, through the reduction of salicylic acid accumulation or activity, generalized severe disease-susceptibility occurs. Therefore, SAR appears to be an essential component of the defensive repertoire that ensures plant health in nature. Chemicals that activate SAR in the field, as well as crop varieties with constitutive SAR gene expression, will provide new solutions to disease problems for growers in the near future.

Acquired resistance is an important component of the complex disease resistance mechanism in plants, which can result from either pathogen infection or treatment with synthetic, resistance-inducing compounds. In this study, Arabidopsis, a tractable genetic system, is shown to develop resistance to a bacterial and a fungal pathogen following 2,6-dichloroisonicotinic acid (INA) treatment. Three proteins that accumulated to high levels in the apoplast in response to INA treatment were purified and characterized. Expression of the genes corresponding to these proteins was induced by INA, pathogen infection, and salicylic acid, the latter being a putative endogenous signal for acquired resistance. Arabidopsis should serve as a genetic model for studies of this type of immune response in plants.

Systemic acquired resistance is a broad spectrum inducible defense response that is associated with the expression of a set of genes (SAR genes). Expression of one of these genes (PR-1a from tobacco) in transgenic tobacco confers increased tolerance to two oomycete pathogens. A direct role for salicylic acid (SA) in signaling SAR has been established in tobacco by analysis of transgenic tobacco expressing salicylate hydroxylase (SAH, an enzyme that inactivates SA by conversion to catechol). Tobacco plants that express SAH are blocked in the accumulation of SA and the development of SAR when responding lo TMV. Furthermore, both Arabidopsis and tobacco expressing SAH have altered pathogen induced lesion morphology, exemplified by larger spreading lesions. Putative mutants in SAR gene expression were isolated by screening M2 Arabidopsis plants for altered expression of PR-1 and PR-2 or for sensitivity to pathogen infection following INA treatment. The putative mutants all into two major classes,constitutive (cim, constitutive immunity) and non-inducible (nim, non-inducible immunity). Several cim mutants exhibits a disease lesion phenotype in the absence of pathogen.

An Arabidopisis cDNA clone was isolated that encodes a protein similar to the antifungal chitin-binding protein hevein from rubber tree latex. This hevein-like (HEL) mRNA was inducible by either turnip crinkle virus infection or ethylene treatment. In addition, expression was moderately inducible by treatment with the resistance-inducing compounds salicylic acid and 2,6-dichlorisonicotinic acid. The 786-bp cDNA contains an open reading frame of 212 codons. The deduced amino acid sequence contains a putative signal sequence of 21 amino acids followed by a 43-amino-acid cysteine-rich lectin domain and a 129-amino-acid carboxy-terminal domain. The predicted protein is approximately 70% identical to hevein, to the wound-inducible WIN1 and WIN2 proteins from potato, and to PR-4, a pathogenesis-related protein from tobacco.