Fenoxaprop-P-ethyl Disrupts Lipid Homeostasis in Rice Seedlings: A Multiomics Study Linking the Inhibition of Acetyl-Coenzyme A Carboxylase with a Coordinated Repression of Fatty Acid Elongation Processes.
TL;DR
It is proposed that FE disrupts lipid homeostasis via "cascade inhibition of lipid metabolism", where suppression of fatty acid elongation amplifies phytotoxicity.
Abstract
Fenoxaprop-P-ethyl (FE), an acetyl-CoA carboxylase (ACCase) inhibitor, disrupts fatty acid synthesis, but downstream lipid disturbances remain unknown. Here, we performed integrative physiological, enzymatic, lipidomic, and transcriptomic analyses to investigate FE-induced lipid disruption in rice seedlings. Lipidomics revealed that FE decreased total lipid content by ∼35%, mostly reducing free fatty acids, phosphatidylglycerol, and lysophosphatidylethanolamine, particularly long-chain (≥C16) species. KEGG enrichment identified fatty acid elongation as a key pathway, with 32 DEGs predominantly downregulated. Most genes for elongation enzymes (KCS, KCR, HCD, ECR) were downregulated, and six key DEGs were confirmed by qRT-PCR. Enzyme assays showed time-dependent inhibition of these enzymes, peaking at 53-66% on day 7 post-treatment. Multiomics analysis suggested that ACCase inhibition disrupts fatty acid elongation, depleting critical lipids. We propose that FE disrupts lipid homeostasis via "cascade inhibition of lipid metabolism", where suppression of fatty acid elongation amplifies phytotoxicity.