N-Acylethanolamine (NAE) inhibits growthin Arabidopsis thaliana seedlings via ABI3-dependent and -independent pathways

Abstract

N-Acylethanolamines (NAEs) are lipid metabolites derived from the hydrolysis of the membrane phospholipidN-acylphosphatidylethanolamine (NAPE). Recent work in Arabidopsis thaliana seedlings showed that combinedtreatments of NAE 12:0 and ABA inhibited seedling growth synergistically, suggesting low levels of NAE could potentiatethe action of ABA. Here we examined the interplay between compound concentrations, growth inhibition and mutantgenotypes with impaired sensitivities to these regulators. NAE 12:0 and ABA both induced dose-dependent increasesin transcript levels of ABI3, and two ABI3 responsive genes, AtHVA22B and RD29B. Interestingly, even in the absence ofgrowth inhibition, RD29B transcripts were elevated by ABA but not NAE treatment outside the sensitive window forABA/NAE treatment, indicating some differences in the regulation of growth and the modulation of gene expression bythese two compounds. Also noteworthy, the growth of ABA insensitive mutant (abi 3-1) seedlings was inhibited at higherconcentrations of NAE 12:0 but not ABA, suggesting that NAE may act to inhibit early seedling establishment by bothABI3-dependent and ABI3-independent pathways. Collectively our results reinforce the concept that NAE 12:0 interactswith ABA signaling in seedling establishment, but also points to a complexity in this interaction that modulates thesensitivity of young seedlings to phytohormone-mediated growth arrest. © 2011 Landes Bioscience.