Abstract

Endogenous salicylic acid (SA) levels increase and several families of pathogenesis-related genes (including PR1 and PR2) are induced during the resistance response of tobacco to tobacco mosaic virus infection. We have found that at temperatures (32°C) that prevent the induction of PR genes and resistance, the increases in SA levels were eliminated. However, when the resistance response was restored by shifting inoculated plants to lower temperatures, SA levels increased dramatically and preceded PR1 gene expression and necrotic lesion formation associated with resistance. SA was also found in a conjugated form whose levels increased in parallel with the free SA levels. The majority of the conjugated SA is in the form of a SA glucoside. This SA glucoside is active, probably due to its hydrolysis to free SA in the plant.In a search for cellular factors which directly interact with SA, we have detected and partially characterized a SA-binding activity in tobacco leaves. The SA-binding activity is both SDS-and proteinase-sensitive, indicating that it is a protein. The soluble protein has an apparent Kd of 14 mM for SA, which is consistent with the range of physiological concentrations of SA observed during the induction of plant disease responses. Its binding to SA is highly specific. Analogues of SA that are able to induce expression of PR genes and disease resistance strongly competed with SA for binding to this factor. In contrast, biologically inactive analogues could not compete with SA for binding. A partially purified preparation of the SA-binding protein, containing three major protein species and several minor ones, has been obtained.KeywordsSalicylic AcidTobacco Mosaic VirusSalicylic Acid SignalSalicylic Acid LevelSystemic Acquire ResistanceThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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