“…SAR can be induced by the exogenous application of SA (White, 1979) or by chemicals, such as 2,6-dichloroisonicotinic acid (INA; Métraux et al, 1991) or benzo( 1,2,3)t hiad iazole-7-carbot hioc acid S-met h yl ester (Gorlach et al, 1996), that are functional analogs of SA. Elevation of endogenous SA levels has been found near lesion sites during an HR and subsequently in systemic tissues, accompanying the onset of SAR (Malamy et al, 1990(Malamy et al, , 1992Métraux et al, 1990;Rasmussen et al, 1991;Yalpani et al, 1991;Enyedi et al, 1992;Uknes et al, 1993). In addition, transgenic tobacco and Arabidopsis plants expressing nahG, a bacterial gene encoding salicylate hydroxylase (which converts SA to catechol; You et al, 1991), can neither accumulate significant levels of SA nor induce PR gene transcription or SAR in response to pathogen invasion .…”