内质网出口位点处磷脂酰肌醇4-磷酸的形成调节内质网输出。
Phosphatidylinositol 4-phosphate formation at ER exit sites regulates ER export.
作者信息
Blumental-Perry Anna, Haney Charles J, Weixel Kelly M, Watkins Simon C, Weisz Ora A, Aridor Meir
机构信息
Department of Cell Biology, University of Pittsburgh School of Medicine, 3500 Terrace Street, Pittsburgh, Pennsylvania 15261, USA.
出版信息
Dev Cell. 2006 Nov;11(5):671-82. doi: 10.1016/j.devcel.2006.09.001.
The mechanisms that regulate endoplasmic reticulum (ER) exit-site (ERES) assembly and COPII-mediated ER export are currently unknown. We analyzed the role of phosphatidylinositols (PtdIns) in regulating ER export. Utilizing pleckstrin homology domains and a PtdIns phosphatase to specifically sequester or reduce phosphorylated PtdIns levels, we found that PtdIns 4-phosphate (PtsIns4P) is required to promote COPII-mediated ER export. Biochemical and morphological in vitro analysis revealed dynamic and localized PtsIns4P formation at ERES. PtdIns4P was utilized to support Sar1-induced proliferation and constriction of ERES membranes. PtdIns4P also assisted in Sar1-induced COPII nucleation at ERES. Therefore, localized dynamic remodeling of PtdIns marks ERES membranes to regulate COPII-mediated ER export.
目前尚不清楚调节内质网（ER）出口位点（ERES）组装和COPII介导的ER输出的机制。我们分析了磷脂酰肌醇（PtdIns）在调节ER输出中的作用。利用普列克底物蛋白同源结构域和一种PtdIns磷酸酶特异性地隔离或降低磷酸化PtdIns水平，我们发现4-磷酸磷脂酰肌醇（PtsIns4P）是促进COPII介导的ER输出所必需的。生化和形态学体外分析揭示了ERES处动态且局部的PtsIns4P形成。PtdIns4P用于支持Sar1诱导的ERES膜增殖和收缩。PtdIns4P还协助Sar1在ERES处诱导COPII成核。因此，PtdIns的局部动态重塑标记ERES膜以调节COPII介导的ER输出。
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