Salicylic Acid Is a Systemic Signal and an Inducer of Pathogenesis-Related Proteins in Virus-Infected Tobacco

Abstract

Systemic induction of pathogenesis-related (PR) proteins in tobacco, which occurs during the hypersensitive response to tobacco mosaic virus (TMV), may be caused by a minimum 10-fold systemic increase in endogenous levels of salicylic acid (SA). This rise in SA parallels PR-1 protein induction and occurs in TMV-resistant Xanthi-nc tobacco carrying the N gene, but not in TMV-susceptible (nn) tobacco. By feeding SA to excised leaves of Xanthi-nc (NN) tobacco, we have shown that the observed increase in endogenous SA levels is sufficient for the systemic induction of PR-1 proteins. TMV infection became systemic and Xanthi-nc plants failed to accumulate PR-1 proteins at 32 degrees C. This loss of hypersensitive response at high temperature was associated with an inability to accumulate SA. However, spraying leaves with SA induced PR-1 proteins at both 24 and 32 degrees C. SA is most likely exported from the primary site of infection to the uninfected tissues. A computer model predicts that SA should move rapidly in phloem. When leaves of Xanthi-nc tobacco were excised 24 hr after TMV inoculation and exudates from the cut petioles were collected, the increase in endogenous SA in TMV-inoculated leaves paralleled SA levels in exudates. Exudation and leaf accumulation of SA were proportional to TMV concentration and were higher in light than in darkness. Different components of TMV were compared for their ability to induce SA accumulation and exudation: three different aggregation states of coat protein failed to induce SA, but unencapsidated viral RNA elicited SA accumulation in leaves and phloem. These results further support the hypothesis that SA acts as an endogenous signal that triggers local and systemic induction of PR-1 proteins and, possibly, some components of systemic acquired resistance in NN tobacco.

Purification, Cloning, and Expression of a Pathogen Inducible UDP-glucose:Salicylic Acid Glucosyltransferase from Tobacco

“…Tobacco plants (Nicotiana tabacum L. cv Xanthi-nc NN genotype) were grown as described previously (14). SA infiltration or inoculation * The costs of publication of this article were defrayed in part by the payment of page charges.…”

Lipid-derived signals that discriminate wound- and pathogen-responsive isoprenoid pathways in plants: methyl jasmonate and the fungal elicitor arachidonic acid induce different 3-hydroxy-3-methylglutaryl-coenzyme A reductase genes and antimicrobial isoprenoids in Solanum tuberosum L.

“…To further examine the specificity of the response of HMGR genes, several compounds known to induce disease resistance and to activate defense-related genes in plants were tested for their effects on potato hmgl expression. SA and ASA induce pathogenesis-related proteins in plants, and SA appears to function as a signal for systemic acquired resistance in some species (33). SA and its derivatives were tested for elicitor activity at 1, 5, and 10 mM, concentrations that induce resistance in other plant species (34,35).…”

Generation of broad-spectrum disease resistance by overexpression of an essential regulatory gene in systemic acquired resistance

“…In addition, exogenous application of SA or its analogs, such as 2,6-dichloroisonicotinic acid (INA) and benzo(1,2,3)thiadiazole-7-carbothioic acid S-methyl ester has been shown to induce SAR (17,18). Often associated with the acquired resistance response is the induction of a group of pathogenesis-related (PR) genes; the roles of these genes in determining resistance have been inferred based on their expression patterns and sequence information (19)(20)(21)(22), and demonstrated in some cases by observation of enhanced resistance in transgenic plants overexpressing a specific PR gene (23)(24)(25)(26)(27). However, the protection provided by a single PR gene is much narrower than that rendered by full-fledged SAR, and the degree of resistance is much less significant.…”