脂质转移蛋白和翻转酶在膜扩张和细胞器发生中的伙伴关系模型。
A model for a partnership of lipid transfer proteins and scramblases in membrane expansion and organelle biogenesis.
机构信息
Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520.
Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520
出版信息
Proc Natl Acad Sci U S A. 2021 Apr 20;118(16). doi: 10.1073/pnas.2101562118.
The autophagy protein ATG2, proposed to transfer bulk lipid from the endoplasmic reticulum (ER) during autophagosome biogenesis, interacts with ER residents TMEM41B and VMP1 and with ATG9, in Golgi-derived vesicles that initiate autophagosome formation. In vitro assays reveal TMEM41B, VMP1, and ATG9 as scramblases. We propose a model wherein membrane expansion results from the partnership of a lipid transfer protein, moving lipids between the cytosolic leaflets of apposed organelles, and scramblases that reequilibrate the leaflets of donor and acceptor organelle membranes as lipids are depleted or augmented. TMEM41B and VMP1 are implicated broadly in lipid homeostasis and membrane dynamics processes in which their scrambling activities likely are key.
自噬蛋白 ATG2 被提议在自噬体生物发生过程中从内质网 (ER) 转移大量脂质，与 ER 驻留蛋白 TMEM41B 和 VMP1 以及高尔基体衍生小泡中的 ATG9 相互作用，这些小泡起始自噬体形成。体外测定揭示 TMEM41B、VMP1 和 ATG9 为 scramblases。我们提出了一个模型，其中膜的扩张是由脂质转移蛋白的协同作用导致的，该蛋白在相邻细胞器的胞质小叶之间移动脂质，而 scramblases 在脂质耗尽或增加时重新平衡供体和受体细胞器膜的小叶。TMEM41B 和 VMP1 广泛参与脂质稳态和膜动力学过程，其 scrambling 活性可能是关键。
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