Cell-suspension cultures of Vitis vinifera L. cv Pinot Noir accumulated resveratrol upon fungal elicitation, and the activity of S-adenosyl-i-methi0nine:trans-caffeoyl-coenzyme A 3-O-methyltransferase (CCoAOMT), yielding feruloyl-COA, increased to a transient maximum at 12 to 15 h. CCoAOMT cDNA was cloned from the elicited cells and was shown to encode a polypeptide highly homologous to CCoAOMTs from cells of Petroselinum species or Zinnia species. The expression of the cDNA i n Escherichia coli revealed that grapevine CCoAOMT methylates both caffeoyland 5-hydroxyferuloyl-coenzyme A and is probably involved in phenolic esterification and lignification. Commercial plant activators induce the disease-resistance response of test plants and are considered to mimic the action of salicylic acid. Among these chemicals, 2,6-dichloroisonicotinic acid and benzo(l,2,3)-thiadiazole-7-carbothioic acid S-methyl ester provoke systemic acquired resistance (SAR) and were also shown to induce the expression of class III chitinase i n grapevine. The SAR response is classified by an unchanged phenotype of tissues, but the mechanistic basis is unknown. Treatment of the cultured V. vinifera cells with either fungal elicitor or low concentrations of salicylic acid and 2,6-dichloroisonicotinic acid, respectively, raised the CCoAOMT or stilbene synthase transcript abundance, suggesting that grapevine is capable of the SAR response, whereas benzo(l,2,3)-thiadiazole-7-carbothioic acid S-methyl ester was ineffective. The data imply for the first time (to our knowledge) that the expression of phenylpropanoid genes in grapevine i s induced by SAR activators without phenotypic consequences and suggest a role for CCoAOMT and stilbene synthase in the disease-resistance response leading beyond the leve1 of pathogenesis-related proteins as markers of the SAR.Plants respond to local fungal infection by the activation of various defense measures in the challenged tissues, and the induction of phenylpropanoid pathways appears to play a crucial role in this response (Hahlbrock and Scheel, 1989). The activation causes the short-term accumulation of phenolic metabolites, which might possess potent antimycotic activity as such or may protect the cells indirectly after incorporation into the cell wall. The phenolic materi-