Format

Send to

Choose Destination
Cell. 2017 Aug 24;170(5):939-955.e24. doi: 10.1016/j.cell.2017.07.015. Epub 2017 Aug 10.

Golgi-Resident Gαo Promotes Protrusive Membrane Dynamics.

Author information

1
Department of Pharmacology and Toxicology, University of Lausanne, CH-1011 Lausanne, Switzerland. Electronic address: gonzalo.solis@unil.ch.
2
Department of Pharmacology and Toxicology, University of Lausanne, CH-1011 Lausanne, Switzerland.
3
Department of Pharmacology and Toxicology, University of Lausanne, CH-1011 Lausanne, Switzerland; School of Biomedicine, Far Eastern Federal University, Vladivostok 690950, Russian Federation. Electronic address: vladimir.katanaev@unil.ch.

Abstract

To form protrusions like neurites, cells must coordinate their induction and growth. The first requires cytoskeletal rearrangements at the plasma membrane (PM), the second requires directed material delivery from cell's insides. We find that the Gαo-subunit of heterotrimeric G proteins localizes dually to PM and Golgi across phyla and cell types. The PM pool of Gαo induces, and the Golgi pool feeds, the growing protrusions by stimulated trafficking. Golgi-residing KDELR binds and activates monomeric Gαo, atypically for G protein-coupled receptors that normally act on heterotrimeric G proteins. Through multidimensional screenings identifying > 250 Gαo interactors, we pinpoint several basic cellular activities, including vesicular trafficking, as being regulated by Gαo. We further find small Golgi-residing GTPases Rab1 and Rab3 as direct effectors of Gαo. This KDELR → Gαo → Rab1/3 signaling axis is conserved from insects to mammals and controls material delivery from Golgi to PM in various cells and tissues.

KEYWORDS:

Drosophila melanogaster; G protein coupled receptors; Golgi apparatus; Gαo interactome; KDEL receptor; Rab1/3 GTPases; heterotrimeric G proteins; neurite outgrowth; protrusion formation; vesicular trafficking

PMID:
28803726
DOI:
10.1016/j.cell.2017.07.015
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center