At4g29530 是一种与 PECP1 同源的磷酸乙醇胺磷酸酶，可调节开花时间,The Plant Journal

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At4g29530 是一种与 PECP1 同源的磷酸乙醇胺磷酸酶，可调节开花时间
The Plant Journal ( IF 6.2 ) Pub Date : 2021-06-07 , DOI: 10.1111/tpj.15367
Martin Tannert ₁ , Gerd Ulrich Balcke ₂ , Alain Tissier ₂ , Margret Köck ₁

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磷脂酰胆碱 (PC) 和磷脂酰乙醇胺 (PE) 是膜中最丰富的磷脂。磷脂的生物合成主要通过肯尼迪途径发生。最近的研究表明，通过该途径，胆碱 (Cho) 部分是通过磷酸化碱基N-甲基转移酶将磷酸乙醇胺 (PEtn) 甲基化为磷酸胆碱 (PCho) 而合成的。在拟南芥中，磷酸乙醇胺/磷酸胆碱磷酸酶 1 (PECP1) 被描述为一种酶，它通过在磷酸盐饥饿期间降低 PEtn 水平来调节 Pcho 的合成，以避免消耗能量的甲基化步骤。通过同源性搜索，我们确定了一个基因（At4g29530) 编码来自拟南芥的假定 PECP1 同源物，在植物中具有目前未知的生物学功能。我们发现 At4g29530 不是由磷酸盐饥饿诱导的，主要在叶和花中表达。对无效突变体和过表达系的分析表明，与 PECP1 一样，PEtn 而不是 PCho 是体内底物。头组代谢物的亲水相互作用色谱-耦合质谱分析显示无效突变体中的 PEtn 水平升高，乙醇胺水平降低。At4g29530无效突变体具有早期开花表型，较高的 PC/PE 比率证实了这一点。此外，我们发现 Pcho 水平升高。胆碱水平没有改变，因此结果证实了依赖 PEtn 的途径是产生 Cho 部分的主要途径。我们假设 PEtn 水解酶参与微调代谢途径，并有助于通过甲基化途径防止 Pcho 的能量消耗生物合成。

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At4g29530 is a phosphoethanolamine phosphatase homologous to PECP1 with a role in flowering time regulation

Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) are the most abundant phospholipids in membranes. The biosynthesis of phospholipids occurs mainly via the Kennedy pathway. Recent studies have shown that through this pathway, choline (Cho) moieties are synthesized through the methylation of phosphoethanolamine (PEtn) to phosphocholine (PCho) by phospho-base N-methyltransferase. In Arabidopsis thaliana, the phosphoethanolamine/phosphocholine phosphatase1 (PECP1) is described as an enzyme that regulates the synthesis of PCho by decreasing the PEtn level during phosphate starvation to avoid the energy-consuming methylation step. By homology search, we identified a gene (At4g29530) encoding a putative PECP1 homolog from Arabidopsis with a currently unknown biological function in planta. We found that At4g29530 is not induced by phosphate starvation, and is mainly expressed in leaves and flowers. The analysis of null mutants and overexpression lines revealed that PEtn, rather than PCho, is the substrate in vivo, as in PECP1. Hydrophilic interaction chromatography-coupled mass spectrometry analysis of head group metabolites shows an increased PEtn level and decreased ethanolamine level in null mutants. At4g29530 null mutants have an early flowering phenotype, which is corroborated by a higher PC/PE ratio. Furthermore, we found an increased PCho level. The choline level was not changed, so the results corroborate that the PEtn-dependent pathway is the main route for the generation of Cho moieties. We assume that the PEtn-hydrolyzing enzyme participates in fine-tuning the metabolic pathway, and helps prevent the energy-consuming biosynthesis of PCho through the methylation pathway.

更新日期：2021-06-07

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