Rab1b regulates COPI and COPII dynamics in mammalian cells

Abstract

Rabs GTPases are key regulatory factors that specifically associate to organelles that integrate membrane transport pathways. Rabs, through their interactions with diverse effector proteins, regulate the formation, movement, tethering and fusion of transport carriers (vesicles and/or tubules). The mammalian Rab1b GTPase is required for ER to Golgi transport and interacts with multiple effectors localized at the ER-Golgi interface. Here, we focus on interactions between Rab1b and effectors that play essential roles in COPII and COPI vesicle formation/function. Based on evidence to date, we propose a model of Rab1b action at the ER exit sites.

Figure 1

Rab1b participation in sequential transport stages at the ERES: (A) Formation and budding of COPII vesicles; Rab1b depletion induces COPII vesicle accumulation. (B) Homotypic fusion of COPII vesicles and formation of VTCs: Rab1b co-localizes with these structures. (C and D) Maturation of VTCs: Rab1b recruits GBF1, which induces COPI recruitment required for the forward movement of VTCs to the cis-Golgi. BFA treatment inhibits GBF1 membrane association without disturbing Rab1b recruitment. More details are provided in the text.