N-acylethanolamine (NAE) inhibits growth in Arabidopsis thaliana seedlings via ABI3-dependent and -independent pathways.

N-acylethanolamines (NAEs) are lipid metabolites derived from the hydrolysis of the membrane phospholipid N-acylphosphatidylethanolamine (NAPE). Recent work in Arabidopsis thaliana seedlings showed that combined treatments of NAE 12:0 and ABA inhibited seedling growth synergistically, suggesting low levels of NAE could potentiate the action of ABA. Here we examined the interplay between compound concentrations, growth inhibition and mutant genotypes with impaired sensitivities to these regulators. NAE 12:0 and ABA both induced dose-dependent increases in transcript levels of ABI3, and two ABI3 responsive genes, AtHVA22B and RD29B. Interestingly, even in the absence of growth inhibition, RD29B transcripts were elevated by ABA but not NAE treatment outside the sensitive window for ABA/NAE treatment, indicating some differences in the regulation of growth and the modulation of gene expression by these two compounds. Also noteworthy, the growth of ABA insensitive mutant (abi 3-1) seedlings was inhibited at higher concentrations of NAE 12:0 but not ABA, suggesting that NAE may act to inhibit early seedling establishment by both ABI3-dependent and ABI3-independent pathways. Collectively our results reinforce the concept that NAE12:0 interacts with ABA signaling in seedling establishment, but also points to a complexity in this interaction that modulates the sensitivity of young seedlings to phytohormone-mediated growth arrest.