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 PROTEIN1 (ACBP1) and ACBP2. Here, we show that polyunsaturated linolenoyl‐CoA (18:3‐CoA) regulates RAP2.12 release 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, 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‐CoA‐induced expression of hypoxia‐related genes. In knockout mutants and overexpression lines of LONG‐CHAIN 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.

中文翻译：

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多不饱和亚油酰基-CoA调节拟南芥中ERF-VII介导的缺氧信号传导。

在植物中，洪水淹没会导致缺氧，这会损害能源生产并影响植物的生长，生产力和生存。在拟南芥中缺氧会导致其与质膜锚定的ACYL-COA结合蛋白1（ACBP1）和ACBP2解离，从而引起与AP2.12（RAP2.12）相关的VII组乙烯应答转录因子的核定位。在这里，我们表明多不饱和亚油酸辅酶A（18：3-辅酶A）调节了RAP2.12从质膜的释放。淹没导致18：3-CoA显着增加，但18：0-，18：1-和18：2-CoA显着下降。18：3-CoA的应用促进了绿色荧光蛋白（GFP）融合体RAP2.12-GFP，HYPOXIA-RESERSIVE ERF1-GFP和RAP2.3-GFP的核积累，并增强了缺氧响应基因的转录水平。ACBP1和ACBP2（acbp1 ACBP2-RNAi减少的植物，由acbp1中的ACBP2 RNA干扰产生突变体）降低了对缺氧的耐受性并削弱了18：3-CoA诱导的缺氧相关基因的表达。在长链酰基-COA合酶2（LACS2）和脂肪酸脱饱和酶3（FAD3）的敲除突变体和过表达系中，酰基辅酶A库大小和18：3-辅酶A水平与ERF-VII介导的信号转导和耐缺氧性。这些发现表明，通过调节ACBP-ERF-VII动力学，长链酰基CoAs的多不饱和度是调节植物缺氧信号的重要机制。