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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 #315411

Title: The maize death acids, 10-oxo-11-phytoenoic acid and derivatives, demonstrate specificity in jasmonate-related signaling and defense

Author
item Christensen, Shawn
item KAPLAN, FATMA - University Of Florida
item HUFFAKER, ALISA - University Of California
item SIMS, JAMES - Eth Zurich
item DOEHLEMANN, GUNTHER - Max Planck Society
item Teal, Peter
item SCHMELZ, ERIC - University Of California

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/15/2015
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Plant cellular damage promotes the interaction of lipoxygenases (LOX) with free fatty acids to yield 9- and 13-hydroperoxides which are further metabolized into diverse oxylipins. The enzymatic action of 13-LOX on linolenic acid enables production of 12-oxo-phytodienoic acid (12-OPDA) and its downstream products, jointly known as jasmonates. As signals, jasmonates have related yet distinct roles in the regulation of plant resistance against insect and pathogen attack. An additional and conceptually parallel pathway involving 9-LOX activity on linoleic acid leads to the production of 10-oxo-11-phytoenoic acid (10-OPEA). Despite structural similarity to jasmonates, physiological roles for 10-OPEA have remained unclear. In developing maize (Zea mays) leaves, 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 metabolites, collectively termed ‘death acids’. While typic! ally absent, 10-OPEA becomes highly wound-inducible within fungal-infected tissues. As a direct defense, 10-OPEA suppresses the growth of mycotoxigenic fungi, including Aspergillus flavus and Fusarium verticillioides, and also the insect herbivore Helicoverpa zea. Both 12-OPDA and 10-OPEA equally promote the transcription of numerous defense genes encoding glutathione S-transferases, cytochrome P450s, and pathogenesis-related proteins; however, 10-OPEA activity diverges in the context of reduced protease inhibitor transcript accumulation. Consistent with a role in dying tissue, 10-OPEA exhibits significant potency and specificity in triggering ion leakage and cell death, which is significantly impaired by the cysteine protease inhibitor maize cystatin-9. Unlike widely encountered jasmonates, functions of 10-OPEA and associated death acids are consistent with specialized roles in local defense reactions.