Phosphatidylserine flux into mitochondria unveiled by organelle-targeted Escherichia coli phosphatidylserine synthase PssA.
Phosphatidylserine flux into mitochondria unveiled by organelle-targeted Escherichia coli phosphatidylserine synthase PssA.
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细胞器靶向大肠杆菌磷脂酰丝氨酸合酶 PssA 揭示了磷脂酰丝氨酸流入线粒体。
DOI：
10.1111/febs.15657
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Yasushi Tamura
中科院分区：
文献类型：
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作者：
Hiroya Shiino;Shiina Furuta;Rieko Kojima;Keisuke Kimura;Toshiya Endo;Yasushi Tamura
大多数磷脂在内质网中合成并分布到其他细胞膜。虽然囊泡运输有助于磷脂在内膜系统中的分布，但磷脂究竟如何运输到线粒体膜、从线粒体膜运输到线粒体膜以及在线粒体膜之间运输仍然不清楚。为了深入了解磷脂转运途径进入线粒体，我们表达了大肠杆菌磷脂酰丝氨酸（PS）合酶PssA在各种膜室与不同的膜拓扑结构在酵母细胞缺乏一个唯一的PS合酶（Cho 1）。有趣的是，PssA可以补充损失的Cho 1时，针对内质网（ER），过氧化物酶体，或脂滴膜。合成的PS可以通过线粒体PS脱羧酶Psd 1转化为磷脂酰乙醇胺（PE），这表明在过氧化物酶体中合成的磷脂和低剂量（LD）可以有效地到达线粒体。此外，我们发现，PssA已整合到线粒体内膜（MIM）从基质侧可以部分地补充Cho 1的损失。在MIM中合成的PS也转化为PE，表明PS在MIM中翻转成为PE。这些发现扩展了我们对通过线粒体的细胞内磷脂转运途径的理解。
Most phospholipids are synthesised in the endoplasmic reticulum and distributed to other cellular membranes. Although the vesicle transport contributes to the phospholipid distribution among the endomembrane system, exactly how phospholipids are transported to, from and between mitochondrial membranes remains unclear. To gain insights into phospholipid transport routes into mitochondria, we expressed theEscherichia coliphosphatidylserine (PS) synthase PssA in various membrane compartments with distinct membrane topologies in yeast cells lacking a sole PS synthase (Cho1). Interestingly, PssA could complement loss of Cho1 when targeted to the endoplasmic reticulum (ER), peroxisome, or lipid droplet membranes. Synthesised PS could be converted to phosphatidylethanolamine (PE) by Psd1, the mitochondrial PS decarboxylase, suggesting that phospholipids synthesised in the peroxisomes and low doses (LDs) can efficiently reach mitochondria. Furthermore, we found that PssA which has been integrated into the mitochondrial inner membrane (MIM) from the matrix side could partially complement the loss of Cho1. The PS synthesised in the MIM was also converted to PE, indicating that PS flops across the MIM to become PE. These findings expand our understanding of the intracellular phospholipid transport routes via mitochondria.