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In plants,submergence from flooding causes hypoxia,which impairs energy production and affects plant growth,productivity,and survival.In Arabidopsis,hypoxia induces nuclear localization of the group Ⅶethylene-responsive transcription factor RELATED TO AP2.12 (RAP2.12),following its dissociation from the plasma membrane-anchored ACYL-COA BINDING PROTEIN1 (ACBP1) and ACBP2.Here,we show that polyunsaturated linolenoyl-CoA (18:3-CoA) regulates RAP2.12release from the plasma membrane.Submergence caused a significant increase in 18:3-CoA,but a significant decrease in 18:0-,18:1-,and 18:2-CoA.Application of 18:3-CoA promoted nuclear accumulation of the green fluorescent protein (GFP) fusions RAP2.12-GFP,HYPOXIARESPONSIVE ERF1-GFP,and RAP2.3-GFP,and enhanced transcript levels of hypoxia-responsive genes.Plants with decreased ACBP1 and ACBP2 (acbp1 ACBP2-RNAi,produced by ACBP2 RNA interference in the acbp1 mutant)had reduced tolerance to hypoxia and impaired 18:3-CoAinduced expression of hypoxia-related genes.In knockout mutants and overexpression lines of LONGCHAIN ACYL-COA SYNTHASE2 (LACS2) and FATTY ACID DESATURASE 3 (FAD3),the acyl-CoA pool size and 18:3-CoA levels were closely related to ERF-Ⅶ-mediated signaling and hypoxia tolerance.These findings demonstrate that polyunsaturation of long-chain acyl-CoAs functions as important mechanism in the regulation of plant hypoxia signaling,by modulating ACBP-ERF-Ⅶ dynamics.