SA-ABA antagonism in defense responses

Abstract

Until recently, phytohormones were mostly studied separately. However, recent studies have suggested that the signaling pathways involved are highly interconnected. We recently reported the antagonistic effects of salicylic acid (SA) and abscisic acid (ABA) in the lesion mimic mutants, cpr22 and ssi4. After shifting these mutants from high humidity, where the lesion mimic phenotype is suppressed to permissive low humidity condition, both SA and ABA pathways were up-regulated. However, the increased levels of SA were able to block downstream ABA responses even though ABA signaling genes and endogenous ABA were elevated. Furthermore, these lesion mimic mutants displayed a partial ABA insensitivity with respect to germination, guard cell opening, and water loss. This increased water loss in detached mutant plants could also be mimicked by treating wild type plants with SA. An active SA analog, 5-chloro-salicylic acid also induced enhanced water loss, while an inactive analog, 4-hydroxy-benzoic acid, did not. Here, we report that the biological analogs of SA, the systemic acquired resistance (SAR) activators, BTH (benzo-(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester) and BIT (1,2-benzisothiazol-3(2H)-one1,1-dioxide), did not have the same effect as SA, suggesting that SA may have additional roles to defense, and that SAR activators may not mimic all SA effects.