期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2015
卷号：112
期号：36
页码：11407-11412
DOI：10.1073/pnas.1511131112
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceIn plants, 12-oxo-phytodienoic acid (12-OPDA) and jasmonic acid are key 13-lipoxygenase-derived linolenate oxidation products termed jasmonates that regulate diverse processes in development and innate immunity. A less-studied metabolic pathway branch is generated by 9-lipoxygenase activity on linoleic acid, enabling the production of 10-oxo-11-phytoenoic acid (10-OPEA). In maize, fungal infection by southern leaf blight (Cochliobolus heterostrophus) results in the localized production of 10-OPEA, and a series of related 12- and 14-carbon cyclopente(a)nones, collectively termed "death acids" (DAs). DAs far exceed jasmonates in abundance within infected tissues, display direct phytoalexin activity against biotic agents, mediate defense gene expression, and can promote cytotoxicity resulting in cell death. Collectively DA activities are consistent with specialized local roles in plant defense. Plant damage promotes the interaction of lipoxygenases (LOXs) 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.
