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ARS Home » Southeast Area » Gainesville, Florida » Center for Medical, Agricultural and Veterinary Entomology » Chemistry Research » Research » Publications at this Location » Publication #326485

Research Project: Impact of Climate Change on Plant Defense Responses Induced by Insect Herbivores and Plant Pathogens

Location: Chemistry Research

Title: Maize death acids, 9-lipoxygenase derived cyclopente(a)nones, display activity as cytotoxic phytoalexins and transcriptional mediators

Author
item Christensen, Shawn
item Huffaker, Alisa - University Of California
item Kaplan, Fatma - University Of Florida
item Sims, James - Eth Zurich
item Doehlemann, Gunther - University Of Cologne
item Schmitz, Robert - University Of Georgia
item Kolomiets, Michael - Texas A&m University
item Jander, Georg - Boyce Thompson Institute
item Ni, Xinzhi
item Abdo, Zaid
item Schmelz, Eric - University Of California

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 4/2/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Plant damage promotes the interaction of lipoxygenases (LOX) with fatty acids yielding 9-hydroperoxides, 13-hydroperoxides and complex arrays of oxylipins. The action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, termed jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. A similar pathway involving 9-LOX activity on linolenic and linoleic acid leads to the 12-OPDA positional isomer, 10-oxo-11-phytodienoic acid (10-OPDA) and 10-oxo-11-phytoenoic acid (10-OPEA), respectively; however, physiological roles for 9-LOX cyclopentenones have remained unclear. In developing maize (Zea mays) leaves, southern leaf blight (Cochliobolus heterostrophus) infection results in dying necrotic tissue and the localized accumulation of 10-OPEA, 10-OPDA and a series of related 14- and 12-carbon metabolites, collectively termed ‘death acids’. 10-OPEA accumulation becomes wound-inducible within fungal-infected tissues and at physiologically relevant concentrations acts as a phytoalexin by suppressing the growth of fungi and herbivores including Aspergillus flavus, Fusarium verticillioides, and Helicoverpa zea. Unlike previously established maize phytoalexins, 10-OPEA and 10-OPDA display significant phytotoxicity. Both 12-OPDA and 10-OPEA promote the transcription of defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins. In contrast, 10-OPEA only weakly promotes the accumulation of multiple protease inhibitor transcripts. Consistent with a role in dying tissue, 10-OPEA application promotes cysteine protease activation and cell death which is inhibited by overexpression of the cysteine protease inhibitor maize cystatin-9. Unlike jasmonates, functions for 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.