Polyunsaturated linolenoyl-Co A modulates ERF-Ⅶ mediated hypoxia signaling in Arabidopsis

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 VII ethylene-responsive transcription factor RELATED TO AP2.12(RAP2.12),following its dissociation from the plasma membrane-anchored ACYL-COA BINDING PRO-TEIN1(ACBP1)and ACBP2.Here,we show that polyunsaturated linolenoyl-Co A(18:3-Co A)regulates RAP2.12release from the plasma membrane.Submergence caused a significant increase in 18:3-Co A,but a significant decrease in 18:0-,18:1-,and 18:2-Co A.Application of 18:3-Co A promoted nuclear accumulation of the green fluorescent protein(GFP)fusions RAP2.12-GFP,HYPOXIA-RESPONSIVE 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-Co A-induced expression of hypoxia-related genes.In knockout mutants and overexpression lines of LONG-CHAIN ACYL-COA SYNTHASE2(LACS2)and FATTY ACID DE-SATURASE 3(FAD3),the acyl-Co A pool size and 18:3-Co A levels were closely related to ERF-VII-mediated signaling and hypoxia tolerance.These findings demonstrate that polyunsaturation of long-chain acyl-Co As functions as important mechanism in the regulation of plant hypoxia signaling,by modulating ACBP–ERF-VII dynamics.