Premium
Antisense LOX expression increases herbivore performance by decreasing defense responses and inhibiting growth‐related transcriptional reorganization in Nicotiana attenuata
Author(s) -
Halitschke Rayko,
Baldwin Ian T.
Publication year - 2003
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1046/j.1365-313x.2003.01921.x
Subject(s) - manduca sexta , jasmonic acid , biology , plant defense against herbivory , nicotiana tabacum , methyl jasmonate , oxylipin , biochemistry , manduca , microbiology and biotechnology , botany , gene , insect
Summary Inhibition of jasmonic acid (JA) signaling has been shown to decrease herbivore resistance, but the responsible mechanisms are largely unknown because insect resistance is poorly understood in most model plant systems. We characterize three members of the lipoxygenase (LOX) gene family in the native tobacco plant Nicotiana attenuata and manipulate, by antisense expression, a specific, wound‐ and herbivory‐induced isoform (LOX3) involved in JA biosynthesis. In three independent lines, antisense expression reduced wound‐induced JA accumulation but not the release of green leaf volatiles (GLVs). The impaired JA signaling reduced two herbivore‐induced direct defenses, nicotine and trypsin protease inhibitors (TPI), as well as the potent indirect defense, the release of volatile terpenes that attract generalist predators to feeding herbivores. All these defenses could be fully restored by methyl‐JA (MeJA) treatment, with the exception of the increase in TPI activity, which was partially restored, suggesting the involvement of additional signals. The impaired ability to produce chemical defenses resulted in lower resistance to Manduca sexta attack, which could also be restored by MeJA treatment. Expression analysis using a cDNA microarray, specifically designed to analyze M. sexta ‐induced gene expression in N. attenuata, revealed a pivotal role for LOX3‐produced oxylipins in upregulating defense genes (protease inhibitor, PI; xyloglucan endotransglucosylase/hydrolase, XTH; threonine deaminase, TD; hydroperoxide lyase, HPL), suppressing both downregulated growth genes (RUBISCO and photosystem II, PSII) and upregulated oxylipin genes (α‐dioxygenase, α‐DOX). By genetically manipulating signaling in a plant with a well‐characterized ecology, we demonstrate that the complex phenotypic changes that mediate herbivore resistance are controlled by a specific part of the oxylipin cascade.