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.

Disruption of the Arabidopsis Defense Regulator Genes SAG101, EDS1, and PAD4 Confers Enhanced Freezing Tolerance

In Arabidopsis, three lipase-like regulators, SAG101, EDS1, and PAD4, act downstream of resistance protein-associated defense signaling. Although the roles of SAG101, EDS1, and PAD4 in biotic stress have been extensively studied, little is known about their functions in plant responses to abiotic stresses. Here, we show that SAG101, EDS1, and PAD4 are involved in the regulation of freezing tolerance in Arabidopsis. With or without cold acclimation, the sag101, edsl, and pad4 single mutants, as well as their double mutants, exhibited similarly enhanced tolerance to freezing temperatures. Upon cold exposure, the sag101, edsl, and pad4 mutants showed increased transcript levels of C-REPEAT/DRE BINDING FACTORs and their regulons compared with the wild type. Moreover, freezing-induced cell death and accumulation of hydrogen peroxide were ameliorated in sag101, edsl, and pad4 mutants. The sag101, edsl, and pad4 mutants had much lower salicylic acid （SA） and diacylglycerol （DAG） contents than the wild type, and exogenous application of SA and DAG compromised the freezing tolerance of the mutants. Furthermore, SA suppressed the cold-induced expression of DGATs and DGKs in the wild-type leaves. These findings indicate that SAG101, EDS1, and PAD4 are involved in the freezing response in Arabidopsis, at least in part, by modulating the homeostasis of SA and DAG.