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首页> 外文期刊>Molecular biology of the cell >ADP-ribosylation factor/COPI-dependent events at the endoplasmic reticulum-Golgi interface are regulated by the guanine nucleotide exchange factor GBF1
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ADP-ribosylation factor/COPI-dependent events at the endoplasmic reticulum-Golgi interface are regulated by the guanine nucleotide exchange factor GBF1

机译：内质网-高尔基体界面的ADP-核糖基化因子/ COPI依赖性事件受鸟嘌呤核苷酸交换因子GBF1调节

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ADP-ribosylation factor (ARF) mediated recruitment of COPI to membranes plays a central role in transport between the endoplasmic reticulum. (ER) and the Golgi. The activation of ARFs is mediated by guanine nucleotide exchange factors (GEFs). Although several ARF-GEFs have been identified, the transport steps in which they function are still poorly understood. Here we report that GBF1, a member of the Sec7-domain family of GEFs, is responsible for the regulation of COPI-mediated events at the ER-Golgi interface. We show that GBF1 is essential for the formation, differentiation, and translocation of pre-Golgi intermediates and for the maintenance of Golgi integrity. We also show that the formation of transport-competent ER-to-Golgi intermediates proceeds in two stages: first, a COPI-independent event leads to the formation of an unstable compartment, which is rapidly reabsorbed in the absence of GBF1 activity. Second, the association of GBF1 with this compartment allows COPI recruitment and leads to its maturation into transport intermediates. The recruitment of GBF1 to this compartment is specifically inhibited by brefeldin A. Our findings imply that the continuous recruitment of GBF1 to spatially differentiated membrane domains is required for sustained membrane remodeling that underlies membrane traffic and Golgi biogenesis. [References: 49]
机译：ADP-核糖基化因子（ARF）介导的COPI募集到膜在内质网之间的运输中起着核心作用。 （ER）和高尔基。 ARF的激活是由鸟嘌呤核苷酸交换因子（GEF）介导的。尽管已鉴定出几种ARF-GEF，但对其功能的转运步骤仍知之甚少。在这里，我们报告说，GBF1是GEFs的Sec7域家族的成员，负责在ER-高尔基体界面调控COPI介导的事件。我们表明，GBF1对于前高尔基体的形成，分化和易位以及维持高尔基体完整性至关重要。我们还表明，具有运输能力的ER到高尔基体中间体的形成分两个阶段进行：首先，独立于COPI的事件导致形成不稳定的区室，该区室在没有GBF1活性的情况下会迅速被重吸收。其次，GBF1与该小室的结合允许COPI募集并导致其成熟成为运输中间体。布雷菲德菌素A特异性抑制GBF1募集到该区室。我们的发现表明，持续进行GBF1募集到空间分化的膜结构域是持续的膜重塑所必需的，而膜重塑是膜运输和高尔基生物发生的基础。 [参考：49]

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