Role of Rab1b in COPII dynamics and function

Eur J Cell Biol. 2011 Apr;90(4):301-11. doi: 10.1016/j.ejcb.2010.10.001. Epub 2010 Nov 18.


In eukaryotic cells, proteins destined for secretion are translocated into the endoplasmic reticulum (ER) and packaged into so-called COPII-coated vesicles. In the ER exit sites (ERES), COPII has the capacity of deforming the lipid bilayer, where it modulates the selective sorting and concentration of cargo proteins. In this study, we analyze the involvement of Rab1b in COPII dynamics and function by expressing either the Rab1b negative-mutant (Rab1N121I) or the Rab1b GTP restricted mutant (Rab1Q67L), or performing short interference RNA-based knockdown. We show that Rab1b interacts with the COPII components Sec23, Sec24 and Sec31 and that Rab1b inhibition changes the COPII phenotype. FRAP assays reveal that Rab1b modulates COPII association/dissociation kinetics at the ERES interface. Furthermore, Rab1b inhibition delays cargo sorting at the ER exit sites. We postulate that Rab1b is a key regulatory component of COPII dynamics and function.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • COP-Coated Vesicles / genetics
  • COP-Coated Vesicles / metabolism*
  • COP-Coated Vesicles / physiology
  • Endoplasmic Reticulum / genetics
  • Endoplasmic Reticulum / metabolism
  • HEK293 Cells
  • Humans
  • Protein Transport / genetics
  • RNA, Small Interfering / genetics
  • Rats
  • rab1 GTP-Binding Proteins / genetics
  • rab1 GTP-Binding Proteins / metabolism*


  • RNA, Small Interfering
  • Rab1B protein, human
  • rab1 GTP-Binding Proteins