Phosphatidylinositol 4-phosphate formation at ER exit sites regulates ER export
Phosphatidylinositol 4-phosphate formation at ER exit sites regulates ER export
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DOI：
10.1016/j.devcel.2006.09.001
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发表时间：
2006-11-01
影响因子：
11.8
通讯作者：
Aridor, Meir
中科院分区：
文献类型：
--
作者：
Blumental-Perry, Anna;Haney, Charles J.;Aridor, Meir
调节内质网（ER）出口位点（ERES）组装和COPII介导的ER输出的机制目前尚不清楚。我们分析了磷脂酰肌醇（PtdIns）在调节ER输出中的作用。利用pleckstrin同源结构域和PtdIns磷酸酶特异性螯合或降低磷酸化PtdIns水平，我们发现PtdIns 4-磷酸（PtsIns 4P）是促进COPII介导的ER输出所必需的。生物化学和形态学体外分析显示，动态和本地化的PtsIns 4P形成在ERES。PtdIns 4P用于支持Sar 1诱导的ERES膜的增殖和收缩。PtdIns 4P还有助于在ERES的Sar 1诱导的COPII成核。因此，PtdIns的局部动态重塑标志着ERES膜调节COPII介导的ER输出。
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.