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布氏锥虫:一种研究真核生物磷脂生物合成的模式微生物。

Trypanosoma brucei: a model micro-organism to study eukaryotic phospholipid biosynthesis.

机构信息

Institute of Biochemistry and Molecular Medicine, University of Bern, Bern, Switzerland.

出版信息

FEBS J. 2011 Apr;278(7):1035-46. doi: 10.1111/j.1742-4658.2011.08012.x. Epub 2011 Feb 3.

Abstract

Although the protozoan parasite, Trypanosoma brucei, can acquire lipids from its environment, recent reports have shown that it is also capable of de novo synthesis of all major phospholipids. Here we provide an overview of the biosynthetic pathways involved in phospholipid formation in T. brucei and highlight differences to corresponding pathways in other eukaryotes, with the aim of promoting trypanosomes as an attractive model organism to study lipid biosynthesis. We show that de novo synthesis of phosphatidylethanolamine involving CDP-activated intermediates is essential in T. brucei and that a reduction in its cellular content affects mitochondrial morphology and ultrastructure. In addition, we highlight that reduced levels of phosphatidylcholine inhibit nuclear division, suggesting a role for phosphatidylcholine formation in the control of cell division. Furthermore, we discuss possible routes leading to phosphatidylserine and cardiolipin formation in T. brucei and review the biosynthesis of phosphatidylinositol, which seems to take place in two separate compartments. Finally, we emphasize that T. brucei represents the only eukaryote so far that synthesizes all three sphingophospholipid classes, sphingomyelin, inositolphosphorylceramide and ethanolaminephosphorylceramide, and that their production is developmentally regulated.

摘要

虽然原生动物寄生虫布氏锥虫可以从环境中获取脂质,但最近的报道表明,它也能够从头合成所有主要的磷脂。本文概述了布氏锥虫中参与磷脂形成的生物合成途径,并强调了与其他真核生物相应途径的差异,旨在促进锥虫成为研究脂质生物合成的有吸引力的模式生物。我们表明,涉及 CDP 激活中间产物的磷脂酰乙醇胺的从头合成在布氏锥虫中是必不可少的,其细胞含量的减少会影响线粒体的形态和超微结构。此外,我们强调,磷脂酰胆碱水平的降低会抑制核分裂,表明磷脂酰胆碱的形成在控制细胞分裂中起作用。此外,我们讨论了布氏锥虫中可能导致磷脂丝氨酸和心磷脂形成的途径,并综述了磷脂酰肌醇的生物合成,它似乎发生在两个独立的隔室中。最后,我们强调,布氏锥虫是迄今为止唯一能够合成所有三种鞘磷脂类的真核生物,即神经鞘磷脂、肌醇磷酸神经酰胺和乙醇胺磷酸神经酰胺,并且它们的产生受到发育调控。

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