WY-14,643 and other agonists of the peroxisome proliferator-activated receptor reveal a new mode of action for salicylic acid in soybean disease resistance

Inoculation of soybean (Glycine max [L.] Merr.) cell-suspension cultures wi th avirulent bacteria results in a salicylic acid (SA)-controlled programme d cell death (pcd). To unravel the nature of the SA-dependent step in pcd, a screening procedure for complementing compounds was performed. Diverse ch emicals that are well known as activating ligands for orphan receptors in a nimals, particularly receptors of the PPAR (peroxisome proliferator-activat ed receptor) subfamily, were found to be active. These include the compound s WY-14643, flufenamic acid. LY-171883, tolbutamide, indomethacin and clofi brate. A new marker gene (DD-CA9) from soybean that is induced in the hyper sensitive reaction by SA and by PPAR ligands was isolated by differential d isplay, and showed homology to antifungal lectins. In plants, SA is also in volved in a signal transduction pathway leading to systemic acquired resist ance (SAR). The PPAR ligands which act on the pcd pathway for plant resista nce induce a beta -1,3-glucanase gene in soybean at high concentrations but do not induce marker genes of the SAR pathway such as the PR-I gene in tob acco or Arabidopsis. Thus SA seems to act on two independent plant defence pathways that can now be separately activated by synthetic compounds. We pr opose a model for the control of pcd by SA in soybean, in which SA induces the transcription of (novel) genes required for the final completion of the cell death program.