The PPR protein RARE1-mediated editing of chloroplast accD transcripts is required for fatty acid biosynthesis and heat tolerance in Arabidopsis.
The PPR protein RARE1-mediated editing of chloroplast accD transcripts is required for fatty acid biosynthesis and heat tolerance in Arabidopsis.
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PPR 蛋白 RARE1 介导的叶绿体 accD 转录本编辑是拟南芥脂肪酸生物合成和耐热性所必需的
DOI：
10.1016/j.xplc.2022.100461
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发表时间：
2023-01-09
影响因子：
10.5
通讯作者：
Xiao, Lang-Tao
中科院分区：
文献类型：
--
作者：
Huang, Chao;Liu, Dan;Li, Zi-Ang;Molloy, David P.;Luo, Zhou-Fei;Su, Yi;Li, Hai-Ou;Liu, Qing;Wang, Ruo-Zhong;Xiao, Lang-Tao
据报道，拟南芥叶绿体accD转录物经历RNA编辑，并且accD-C794 RNA编辑的丧失在正常条件下不影响植物生长。到目前为止，accD-C794编辑的确切生物学作用仍然难以捉摸。在这里，我们揭示了accD-C794编辑在热应激反应中的意想不到的作用。缺失accD-C794编辑导致在热胁迫下叶绿体基因表达降低的黄色和矮化表型，并且人工改善C794编辑的accD基因表达增强拟南芥的耐热性。这些数据表明accD-C794编辑赋予植物耐热性。我们还发现，用乙酰辅酶A羧化酶（ACCase）的产物处理可以减轻突变体的表型特征，并表明ACCase α-亚基的CAC 3基因突变与热胁迫下的侏儒症有关。这些观察结果表明，accD-C794编辑缺陷可能是ACC酶活性降低的内在原因，从而导致热敏感性。ACCase催化脂肪酸（FA）从头生物合成的关键步骤。FA含量分析显示，与野生型相比，不饱和油酸（C18：1）和亚油酸（C18：2）在accD-C794编辑缺陷突变体中较低，但在C794编辑的accD过表达植物中较高。补充外源C18：1和C18：2可以挽救突变体表型，表明这些FA在热胁迫耐受中起重要作用。透射电子显微镜观察表明，热胁迫严重影响accD编辑缺陷突变体的膜结构，但在accD过表达植物。这些结果提供了第一个证据表明，accD-C794编辑调节FA生物合成，以维持热应激下的膜结构稳态。拟南芥叶绿体accD转录物经历RNA编辑。accD-C794位点的编辑效率与植物耐热性呈正相关。编辑accD-C794通过调节ACC酶活性和脂肪酸含量来维持膜结构稳态，从而赋予耐热性。
It has been reported that Arabidopsis chloroplast accD transcripts undergo RNA editing and that loss of accD-C794 RNA editing does not affect plant growth under normal conditions. To date, the exact biological role of accD-C794 editing has remained elusive. Here, we reveal an unexpected role for accD-C794 editing in response to heat stress. Loss of accD-C794 editing results in a yellow and dwarf phenotype with decreased chloroplast gene expression under heat stress, and artificial improvement of C794-edited accD gene expression enhances heat tolerance in Arabidopsis. These data suggest that accD-C794 editing confers heat tolerance in planta. We also found that treatment with the product of acetyl coenzyme A carboxylase (ACCase) could allay mutant phenotypic characteristics and showed that a mutation in the CAC3 gene for the α-subunit of ACCase was associated with dwarfism under heat stress. These observations indicate that defective accD-C794 editing may be intrinsic to reduced ACCase activity, thereby contributing to heat sensitivity. ACCase catalyzes the committed step of de novo fatty acid (FA) biosynthesis. FA content analysis revealed that unsaturated oleic (C18:1) and linoleic acids (C18:2) were low in the accD-C794 editing-defective mutant but high in the C794-edited accD-overexpressing plants compared with the wild type. Supplying exogenous C18:1 and C18:2 could rescue the mutant phenotype, suggesting that these FAs play an essential role in tolerance to heat stress. Transmission electron microscopy observations showed that heat stress seriously affected the membrane architecture in accD editing-defective mutants but not in accD-overexpressing plants. These results provide the first evidence that accD-C794 editing regulates FA biosynthesis for maintenance of membrane structural homeostasis under heat stress. Arabidopsis chloroplast accD transcripts undergo RNA editing. Editing efficiency of the accD-C794 site is positively correlated with plant heat tolerance. Editing of accD-C794 confers heat tolerance by regulating ACCase activity and fatty acid content for the maintenance of membrane structural homeostasis.
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