期刊
EMBO JOURNAL
卷 31, 期 13, 页码 2869-2881出版社
WILEY
DOI: 10.1038/emboj.2012.134
关键词
endomembrane signalling; G-protein-coupled receptor; Golgi complex; KDEL receptor
资金
- Telethon (Italy) [S00068TELU]
- AIRC (Italy)
- Italian Foundation for Cystic Fibrosis (Italy)
- MIUR (Italy)
- AIRC [IG 11652]
- Fondazioni per il Sud
- Fondazioni Bancarie Abruzzesi
- Fondazione Negri Sud ONLUS
Membrane trafficking involves large fluxes of cargo and membrane across separate compartments. These fluxes must be regulated by control systems to maintain homoeostasis. While control systems for other key functions such as protein folding or the cell cycle are well known, the mechanisms that control secretory transport are poorly understood. We have previously described a signalling circuit operating at the Golgi complex that regulates intra-Golgi trafficking and is initiated by the KDEL receptor (KDEL-R), a protein previously known to mediate protein recycling from the Golgi to the endoplasmic reticulum (ER). Here, we investigated the KDEL-R signalling mechanism. We show that the KDEL-R is predicted to fold like a G-protein-coupled receptor (GPCR), and that it binds and activates the heterotrimeric signalling G-protein G alpha(q/11) which, in turn, regulates transport through the Golgi complex. These findings reveal an unexpected GPCR-like mode of action of the KDEL-R and shed light on a core molecular control mechanism of intra-Golgi traffic. The EMBO Journal (2012) 31, 2869-2881. doi: 10.1038/emboj.2012.134; Published online 11 May 2012
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