| Abstract | Systemic acquired resistance (SAR) is a long-lasting, broad-spectrum disease resistance that arises throughout a plant, including non-infected tissue, upon localized exposure to a microbe that causes necrosis. Induction of SAR is accompanied by the accumulation of salicylic acid (SA) and is ultimately characterized by the upregulation of Pathogenesis-Related (PR) genes, including the SAR marker gene PR-1. Direct transcriptional control of PR-1 is governed by the TGA2 clade of transcription factors. TGA2, the archetypical member of this clade, demonstrates a unique dichotomy in that it is essential for mediating the repression of PR-1 in resting tissues, yet is also a requisite for activating this gene in SA-stimulated cells. TGA2 is at all times positioned on the PR-1 promoter and constitutes a point of integration for the genetic regulatory information, including that transmitted by transcriptional cofactors, most notably Nonexpresser of Pathogenesis-Related (PR) genes 1 (NPR1). Although the coactivator NPR1 is recognized as THE key regulator of PR-1 gene expression, activation of PR-1 is contingent upon its incorporation into a transactivating enhanceosome complex nucleated by TGA2. |
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