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Entry URI http://metadb.riken.jp/db/SciNetS_ria224i/cria224u4ria224u16880402i
Entry name Wang Yuh-Shuh et al. 2006 Aug. Proc. Natl. Acad. Sci. U.S.A. 103(32):12197-202.
Title Manipulation of Arabidopsis fatty acid amide hydrolase expression modifies plant growth and sensitivity to N-acylethanolamines.
Authors Blancaflor Elison B|Chapman Kent D|Kilaru Aruna|Shrestha Rhidaya|Venables Barney J|Wang Yuh-Shuh|Wiant William
Abstract In vertebrates, the endocannabinoid signaling pathway is an important lipid regulatory pathway that modulates a variety of physiological and behavioral processes. N-Acylethanolamines (NAEs) comprise a group of fatty acid derivatives that function within this pathway, and their signaling activity is terminated by an enzyme called fatty acid amide hydrolase (FAAH), which hydrolyzes NAEs to ethanolamine and their corresponding free fatty acids. Bioinformatic approaches led to the identification of plant homologues of FAAH that are capable of hydrolyzing NAEs in vitro. To better understand the role of NAEs in plants, we identified T-DNA knockouts to Arabidopsis FAAH (AtFAAH; At5g64440) and generated plants overexpressing AtFAAH. Here we show that seeds of AtFAAH knockouts had elevated levels of endogenous NAEs, and seedling growth was hypersensitive to exogenously applied NAE. On the other hand, seeds and seedlings of AtFAAH overexpressors had lower endogenous NAE content, and seedlings were less sensitive to exogenous NAE. Moreover, AtFAAH overexpressors displayed enhanced seedling growth and increased cell size. AtFAAH expression and FAAH catalytic activity increased during seed germination and seedling growth, consistent with the timing of NAE depletion during seedling establishment. Collectively, our results show that AtFAAH is one, but not the only, modulator of endogenous NAE levels in plants, and that NAE depletion likely participates in the regulation of plant growth.
Pubmed ID 16880402
Journal Proceedings of the National Academy of Sciences of the United States of America
Volume 103
Issue 32
Pages 12197-202
Publication date 2006 Aug
Num of phenotype gene 0