Regulation of Golgi structure and secretion by receptor-induced G protein βγ complex translocation

We show that receptor induced G protein βγ subunit translocation from the plasma membrane to the Golgi allows a receptor to initiate fragmentation and regulate secretion. A lung epithelial cell line, A549, was shown to contain an endogenous translocating G protein γ subunit and exhibit receptor-indu...

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Published in:Proceedings of the National Academy of Sciences - PNAS 2010-06, Vol.107 (25), p.11417-11422
Main Authors: Saini, Deepak Kumar, Karunarathne, W.K. Ajith, Angaswamy, Nataraju, Saini, Deepti, Cho, Joon-Ho, Kalyanaraman, Vani, Gautam, Narasimhan
Format: Article
Language:English
Subjects:
Agonists
Animals
Biological Sciences
Cell Line, Tumor
Cell lines
Cell membranes
Genes, Dominant
Golgi Apparatus - metabolism
GTP-Binding Protein beta Subunits - metabolism
GTP-Binding Protein gamma Subunits - metabolism
HeLa cells
Humans
Insulin - metabolism
Insulin secretion
Mice
Microscopy, Fluorescence - methods
Microtubules - metabolism
Phospholipase C beta - metabolism
Physiological regulation
Polycystic kidney diseases
Protein Kinase C - metabolism
Protein subunits
Protein Transport
Receptors
Receptors, Muscarinic - metabolism
Secretion
Signal Transduction
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Summary:We show that receptor induced G protein βγ subunit translocation from the plasma membrane to the Golgi allows a receptor to initiate fragmentation and regulate secretion. A lung epithelial cell line, A549, was shown to contain an endogenous translocating G protein γ subunit and exhibit receptor-induced Golgi fragmentation. Receptor-induced Golgi fragmentation was inhibited by a shRNA specific to the endogenous translocating γ subunit. A kinase defective protein kinase D and a phospholipase C β inhibitor blocked receptor-induced Golgi fragmentation, suggesting a role for this process in secretion. Consistent with βγ translocation dependence, fragmentation induced by receptor activation was inhibited by a dominant negative nontranslocating γ3. Insulin secretion was shown to be induced by muscarinic receptor activation in a pancreatic β cell line, NIT-1. Induction of insulin secretion was also inhibited by the dominant negative γ3 subunit consistent with the Golgi fragmentation induced by βγ complex translocation playing a role in secretion.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1003042107