Salicylic Acid, Ethylene, and Pathogen Resistance in Tobacco. Paul Silverman. AgBiotech Center, Cook College, P.O. Box 231, Rutgers University, New Brunswick, NJ 08903-0231 U.S.A. Etta Nuckles,(2) Xiang Sheng Ye,(2) Joseph Kuc,(2) and Ilya Raskin(1). (1)AgBiotech Center, Cook College, P.O. Box 231, Rutgers University, New Brunswick, NJ 08903-0231 U.S.A.; (2)Department of Plant Pathology, University of Kentucky, Lexington, KY 40546-0091 U.S.A. MPMI 6:775-781. Accepted 1 July 1993. Copyright 1993 The American Phytopathological Society.

Salicylic acid (SA) plays an important regulatory role in the resistance response of N-gene tobacco to tobacco mosaic virus (TMV). To determine whether SA accumulation following inoculation with a necrotizing pathogen is a generalized phenomenon, endogenous SA levels were quantified following inoculation of two species of Nicotiana with viral, bacterial, and fungal pathogens. In Xanthi-nc (NN) and Xanthi (nn) cultivars of Nicotiana tabacum, tobacco necrosis virus produced necrotic lesions and a more than 28-fold increase in total SA (the sum of free and Beta-O-d-glucosyl SA) within 96 hr. Significant increases in SA were also observed in Nicotiana sylvestris inoculated with a mutant TMV strain capable of producing necrotic lesions in this tobacco species. Infiltration of Xanthi-nc and Xanthi tobacco leaves with Pseudomonas syringae pv. tomato also produced a 100-fold increase in total SA within 72 hr. Stem injection with blue mold (Peronospora tabacina) sporangia produced 3.6- and 18.8-fold increases of free and total SA, respectively, in previously uninfected leaves, which coincided with an increase in resistance. Exposure of TMV-inoculated tobacco leaf disks to ethylene (10 μl/L) resulted in a reduction in SA accumulation. However, an inhibitor of ethylene action, 2,5-norbornadiene, did not produce a significant change in SA accumulation in TMV-inoculated leaf tissues. The relatively minor negative effect of ethylene on SA production suggests that ethylene is not directly involved in the signal transduction pathway that leads to SA accumulation and export from the tissues infected with necrotizing pathogens.