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Abstract

Plants release into the atmosphere large quantities of volatile organic compounds (VOCs) of which methanol (MeOH), a putative waste product, is the second most abundant. With on-line proton-transfer-reaction mass spectrometry (PTR-MS), we demonstrate that when Manduca sexta larvae attack Nicotiana attenuata plants, the wound-induced release of MeOH dramatically increases. The sustained MeOH emission 24 h after herbivore feeding is already substantially greater than the release of the well-characterized green leaf VOC, E-2-hexenal. Herbivore attack and treatment of puncture wounds with larval oral secretions (OS) increase transcript accumulation and activity of leaf pectin methylesterases (PMEs), and decrease the degree of pectin methylation, as determined by 1H-NMR; therefore, we propose that the released MeOH originates from the activation of PMEs by herbivore attack. The herbivore- and OS-elicited MeOH results not from the activity of previously characterized elicitors in OS but from a pH shift at the wound site when larval OS (pH 8.5-9.5) are introduced into the wounds during feeding. Applying MeOH to plants in quantities that mimic the herbivory-elicited release decreases the activity of potent plant defense proteins, trypsin proteinase inhibitors (TPI), and increases the performance of the attacking larvae. The pH of lepidopteran larvae regurgitants is commonly very high, and the MeOH released during feeding which is elicited by the pH change at the wound site functions as a quantitative signal that influences the outcome of the plant-herbivore interaction.