Dissection of the Salicylic Acid Signaling Pathway in Tobacco. Jocelyn Malamy. Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers, The State University of New Jersey, Piscataway, NJ 08855 U.S.A. Paloma Sanchez-Casas, Jacek Hennig, Ailan Guo, and Daniel F. Klessig. Waksman Institute and Department of Molecular Biology and Biochemistry, Rutgers, The State University of New Jersey, Piscataway, NJ 08855 U.S.A. MPMI 9:474-482. Accepted 9 April 1996. Copyright 1996 The American Phytopathological Society.

Certain chemicals induce the accumulation of pathogene-sis-related (PR) proteins and enhance resistance to tobacco mosaic virus (TMV) in tobacco at the application site. These compounds include polyacrylic acid (PAA), thia-mine, L-(-amino butyric acid, barium chloride, 2-thiouracil, (-1,4-endoxylanase and 2,6-dichloroisonicotinic acid (INA). Because there is considerable evidence that salicylic acid (SA) is an endogenous signal leading to PR gene expression and enhanced resistance following TMV infection, we evaluated these chemicals to see if they act via SA. We report here that all of the compounds tested except INA induced stable accumulation of the glucoside of SA (SAG), probably via transient or low level production of SA. Thiamine induction of PR-1 gene expression and enhanced resistance to TMV was significantly reduced in salicylate hydroxylase-producing transgenic plants which are unable to accumulate SA. In contrast, induction of PR-1 gene expression and enhanced resistance to TMV by PAA was similar in the transgenic and wild-type plants. Furthermore, thiamine induction of SAG accumulation was blocked at elevated temperatures, whereas PAA was still effective. This suggests the presence of multiple pathways that lead to defense responses, one of which is independent of SA. As PAA, thiamine, and INA enter the pathway(s) leading to PR-1 gene expression and enhanced resistance via distinct mechanisms, they should provide chemical tools for dissection of these pathways.