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Role of RKTG, a novel Golgi localized receptor, in Gβγ regulated transport of secretory proteins from the Golgi to the plasma membrane (604.4)
Author(s) -
Hewavitharana Thamara,
Wedegaertner Philip
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.604.4
Subject(s) - golgi apparatus , microbiology and biotechnology , secretory pathway , signal transduction , protein subunit , chemistry , biology , endoplasmic reticulum , biochemistry , gene
Recent studies have revealed a role for G protein betagamma signaling at the Golgi via protein kinase D (PKD) regulating fission of plasma membrane (PM) destined secretory vesicles from the trans Golgi network (TGN). The mechanism by which the Gbetagamma subunits are recruited to and activated at the Golgi in this process remains elusive. Recent studies reveal that a newly characterized Golgi localized, membrane protein belonging to the Progestin and AdipoQ Receptor (PAQR) family, RKTG (Raf Kinase Trapping to the Golgi), interacts with the Gbeta subunit and sequesters Gbetagamma to the Golgi thereby regulating the functions of Gbetagamma. Here we show that over expression of RKTG causes vesiculation of the Golgi, while a Gbeta binding mutant of RKTG does not cause vesiculation. Also, the C‐terminal fragment of GRK2 (GRK2ct), which interacts with, and inhibits Gbetagamma signaling, and Gallein, a small molecule inhibitor of Gbetagamma, were both able to inhibit Golgi vesiculation in the presence of RKTG. Furthermore, a dominant negative form of PKD (PKD‐DN) and a pharmacological inhibitor of PKD, Go6976, also inhibited RKTG mediated vesiculation of the Golgi. Collectively, these results reveal a novel role for the newly characterized, Golgi localized RKTG receptor, in regulating Gbetagamma at the Golgi, thus controlling Golgi to PM protein transport via the Gbetagamma‐PKD signaling pathway. Grant Funding Source : NIH GM056444