N-acylethanolamine metabolism interacts with abscisic acid signaling in Arabidopsis thaliana seedlings

被引:52
|
作者
Teaster, Neal D.
Motes, Christy M.
Tang, Yuhong
Wiant, William C.
Cotter, Matthew Q.
Wang, Yuh-Shuh
Kilaru, Aruna
Venables, Barney J.
Hasenstein, Karl H.
Gonzalez, Gabriel
Blancaflor, Elison B.
Chapman, Kent D. [1 ]
机构
[1] Univ N Texas, Dept Biol Sci, Ctr Plant Lipid Res, Denton, TX 76203 USA
[2] Samuel Roberts Noble Fdn Inc, Div Plant Biol, Ardmore, OK 73401 USA
[3] Univ Louisiana, Dept Biol, Lafayette, LA 70504 USA
来源
PLANT CELL | 2007年 / 19卷 / 08期
关键词
D O I
10.1105/tpc.106.048702
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
N-Acylethanolamines (NAEs) are bioactive acylamides that are present in a wide range of organisms. In plants, NAEs are generally elevated in desiccated seeds, suggesting that they may play a role in seed physiology. NAE and abscisic acid (ABA) levels were depleted during seed germination, and both metabolites inhibited the growth of Arabidopsis thaliana seedlings within a similar developmental window. Combined application of low levels of ABA and NAE produced a more dramatic reduction in germination and growth than either compound alone. Transcript profiling and gene expression studies in NAE-treated seedlings revealed elevated transcripts for a number of ABA-responsive genes and genes typically enriched in desiccated seeds. The levels of AB13 transcripts were inversely associated with NAE-modulated growth. Overexpression of the Arabidopsis NAE degrading enzyme fatty acid amide hydrolase resulted in seedlings that were hypersensitive to ABA, whereas the ABA-insensitive mutants, abi1-1, abi2-1, and abi3-1, exhibited reduced sensitivity to NAE. Collectively, our data indicate that an intact ABA signaling pathway is required for NAE action and that NAE may intersect the ABA pathway downstream from ABA. We propose that NAE metabolism interacts with ABA in the negative regulation of seedling development and that normal seedling establishment depends on the reduction of the endogenous levels of both metabolites.
引用
收藏
页码:2454 / 2469
页数:16
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