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Metabolism and Actions of N‐Acylethanolamines in Seedling Development
Author(s) -
Chapman Kent,
Keereetaweep Jantana,
Blancaflor Elison
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.366.4
Subject(s) - seedling , abscisic acid , biology , linoleic acid , seed dormancy , cotyledon , arabidopsis thaliana , polyunsaturated fatty acid , biochemistry , lipid signaling , botany , germination , dormancy , fatty acid , enzyme , gene , mutant
N‐Acylethanolamines NAEs are fatty acid derivatives linked to ethanolamine via an amide bond. In seeds of most plants including Arabidopsis thaliana, NAEs with linolenic (18:3) and linoleic (18:2) acids together make up more than 70% of the total NAE pool, and they both decline precipitously to pmol/g‐fr‐wt levels with the progression of seed germination and seedling development. Elevated, exogenous levels of these polyunsaturated NAEs applied within a few days of post‐germinative growth restrict normal seedling establishment with NAE18:2 manifesting marked inhibition of root development and NAE18:3 interfering most conspicuously with normal cotyledon development. Seedling sensitivity to growth inhibition by polyunsaturated NAEs overlaps with the well‐known secondary dormancy stage induced by abscisic acid (ABA) that is believed to support survival from stresses during seedling establishment. Biochemical, genetic and pharmacological evidence indicates that both NAE types can be metabolized by specific lipoxygenase (LOX) isoforms during the course of seedling establishment, leading to a complex array of NAE oxylipin metabolites. Specific ethanolamide oxylipins of the NAEs appear to be attributed to tissue‐specific inhibitory action, and suggest these molecules may participate in the coordinate control of seedling establishment under unfavorable environmental conditions in cooperation with phytohormone and light signaling pathways.