An octadecanoid pathway mutant (JL5) of tomato is compromised in signaling for defense against insect attack

Abstract

The activation of defense genes in tomato plants has been shown to be mediated by an octadecanoic acid-based signaling pathway in response to herbivore attack or other mechanical wounding. We report here that a tomato mutant (JL5) deficient in the activation of wound-inducible defense genes is also compromised in resistance toward the lepidopteran predator Manduca sexta (tobacco hornworm). Thus, we propose the name defenseless1 (def1) for the mutation in the JL5 line that mediates this altered defense response. In experiments designed to define the normal function of DEF1, we found that dell plants are defective in defense gene signaling initiated by prosystemin overexpression in transgenic plants as well as by oligosaccharide (chitosan and polygalacturonide) and polypeptide (systemin) elicitors. Supplementation of plants through their out stems with intermediates of the octadecanoid pathway indicates that def1 plants are affected in octadecanoid metabolism between the synthesis of hydroporoxylinolenic acid and 12-oxo-phytodienoic acid. Consistent with this defect, def1 plants are also compromised in their ability to accumulate jasmonic acid, the end product of the pathway. In response to wounding and the aforementioned elicitors. Taken together, these results show that octadecanoid metabolism plays an essential role in the transduction of upstream wound signals to the activation of antiherbivore plant defenses.