ArfGAP1通过促进衣被蛋白聚合来促进COPI囊泡的形成。
ArfGAP1 promotes COPI vesicle formation by facilitating coatomer polymerization.
作者信息
Shiba Yoko, Luo Ruibai, Hinshaw Jenny E, Szul Tomasz, Hayashi Ryo, Sztul Elizabeth, Nagashima Kunio, Baxa Ulrich, Randazzo Paul A
机构信息
Laboratory of Cellular and Molecular Biology; National Cancer Institute, Bethesda, MD USA.
National Institute of Diabetes and Digestive and Kidney Disease; National Institutes of Health; Bethesda, MD USA.
出版信息
Cell Logist. 2011 Jul-Dec;1(4):139-154. doi: 10.4161/cl.1.4.18896. Epub 2011 Jul 1.
The role of ArfGAP1 in COPI vesicle biogenesis has been controversial. In work using isolated Golgi membranes, ArfGAP1 was found to promote COPI vesicle formation. In contrast, in studies using large unilamellar vesicles (LUVs) as model membranes, ArfGAP1 functioned as an uncoating factor inhibiting COPI vesicle formation. We set out to discriminate between these models. First, we reexamined the effect of ArfGAP1 on LUVs. We found that ArfGAP1 increased the efficiency of coatomer-induced deformation of LUVs. Second, ArfGAP1 and peptides from cargo facilitated self-assembly of coatomer into spherical structures in the absence of membranes, reminiscent of clathrin self-assembly. Third, in vivo, ArfGAP1 overexpression induced the accumulation of vesicles and allowed normal trafficking of a COPI cargo. Taken together, these data support the model in which ArfGAP1 promotes COPI vesicle formation and membrane traffic and identify a function for ArfGAP1 in the assembly of coatomer into COPI.
ArfGAP1在COPI囊泡生物发生中的作用一直存在争议。在使用分离的高尔基体膜的研究中，发现ArfGAP1可促进COPI囊泡形成。相反，在以大单层囊泡（LUVs）作为模型膜的研究中，ArfGAP1作为一种去包被因子抑制COPI囊泡形成。我们着手区分这些模型。首先，我们重新研究了ArfGAP1对LUVs的影响。我们发现ArfGAP1提高了外被体诱导的LUVs变形效率。其次，ArfGAP1和来自货物的肽在无膜情况下促进外被体自组装成球形结构，这类似于网格蛋白的自组装。第三，在体内，ArfGAP1过表达诱导囊泡积累并允许COPI货物正常运输。综上所述，这些数据支持ArfGAP1促进COPI囊泡形成和膜运输的模型，并确定了ArfGAP1在外被体组装成COPI中的作用。
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