GOLGA2 phosphorylated by CDK1 is unable to promote fusion of ER to Golgi transport vesicles with cis-Golgi

USO1 (p115) protein, localizing to membranes of ER to Golgi transport vesicles, binds GOLGA2 (GM130), localizing to membranes of cis-Golgi cisternae. Binding of USO1 to GOLGA2 enables tethering of ER to Golgi transport vesicles to cis-Golgi cisternae, and is facilitated by a Ras-related GTPase RAB1. Fusion of ER to Golgi transport vesicles with cis-Golgi succeeds tethering and depends on STX5 (syntaxin-5). In mitosis, phosphorylation of GOLGA2 by cyclin B-activated CDK1 prevents USO1 docking. This results in cessation of ER to Golgi transport. Halting ER to Golgi transport increases the number of transport vesicles at the expense of Golgi cisternae, since transport vesicles keep budding from the ER but are unable to fuse with Golgi cisternae and deliver their content (Lowe et al. 1998, Seeman et al. 2000, Diao et al. 2008).

USO1（p115）蛋白定位于内质网至高尔基体运输囊泡的膜上，与GOLGA2（GM130）结合，定位至顺式高尔基池的膜。USO1与GOLGA2的结合允许内质网至高尔基体运输囊泡与顺式高尔基池的连接，该过程受RAB1（Ras相关GTPase）的促进作用。内质网与顺式高尔基池的融合成功依赖于STX5（syntaxin-5）。在细胞分裂过程中，由细胞周期蛋白B激活的CDK1对GOLGA2的磷酸化阻止了USO1的对接，从而导致内质网至高尔基体的运输停止。这种运输的停止以牺牲高尔基池为代价，增加了运输囊泡的数量，因为运输囊泡持续从内质网发芽，但无法与高尔基池融合并传递其内容（Lowe等人，1998年，Seeman等人，2000年，Diao等人，2008年）。