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在缺磷条件下,磷酸碱基 N-甲基转移酶 PMT1 和 PMT2 为拟南芥的叶片生长产生磷酸胆碱。

The phospho-base N-methyltransferases PMT1 and PMT2 produce phosphocholine for leaf growth in phosphorus-starved Arabidopsis.

机构信息

Institute of Plant and Microbial Biology, Academia Sinica, Taipei, Taiwan.

Molecular and Biological Agricultural Sciences Program, Taiwan International Graduate Program, Academia Sinica and National Chung Hsing University, Taipei, Taiwan.

出版信息

J Exp Bot. 2022 May 13;73(9):2985-2994. doi: 10.1093/jxb/erab436.

Abstract

Phosphorus (P) is an essential nutrient for plants. Membrane lipid remodeling is an adaptive mechanism for P-starved plants that replaces membrane phospholipids with non-P galactolipids, presumably to retrieve scarce P sources and maintain membrane integrity. Whereas metabolic pathways to convert phospholipids to galactolipids are well-established, the mechanism by which phospholipid biosynthesis is involved in this process remains elusive. Here, we report that phospho-base N-methyltransferases 1 and 2 (PMT1 and PMT2), which convert phosphoethanolamine to phosphocholine (PCho), are transcriptionally induced by P starvation. Shoots of seedlings of pmt1 pmt2 double mutant showed defective growth upon P starvation; however, membrane lipid profiles were unaffected. We found that P-starved pmt1 pmt2 with defective leaf growth had reduced PCho content, and the growth defect was rescued by exogenous supplementation of PCho. We propose that PMT1 and PMT2 are induced by P starvation to produce PCho mainly for leaf growth maintenance, rather than for phosphatidylcholine biosynthesis, in membrane lipid remodeling.

摘要

磷(P)是植物必需的营养物质。膜脂重塑是 P 饥饿植物的一种适应性机制,它用非 P 半乳糖脂取代膜磷脂,大概是为了回收稀缺的 P 源并维持膜的完整性。虽然将磷脂转化为半乳糖脂的代谢途径已经很成熟,但磷脂生物合成如何参与这个过程的机制仍不清楚。在这里,我们报告说,将磷酸乙醇胺转化为磷酸胆碱(PCho)的磷酸碱基 N-甲基转移酶 1 和 2(PMT1 和 PMT2),在 P 饥饿时转录诱导。pmt1 pmt2 双突变体幼苗的地上部分在 P 饥饿时表现出生长缺陷;然而,膜脂谱没有受到影响。我们发现,具有缺陷叶片生长的 P 饥饿 pmt1 pmt2 的 PCho 含量降低,而外源补充 PCho 则可以挽救生长缺陷。我们提出,PMT1 和 PMT2 被 P 饥饿诱导产生 PCho,主要是为了维持叶片生长,而不是为了膜脂重塑中的磷脂酰胆碱生物合成。

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