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Inhibition of serotonin 5-hydroxytryptamine2c receptor function through heterodimerization: receptor dimers bind two molecules of ligand and one G-protein.

Herrick-Davis K, Grinde E, Harrigan TJ, Mazurkiewicz JE

J Biol Chem. 2005 Dec 2; 280(48):40144-51

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Rafael Franco, Universitat de Barcelona, Spain. F1000 Pharmacology & Drug Discovery

05 Sep 2008 | Controversial

I found this article very interesting not only for the content but also for the assertion in the subtitle: "receptor dimers bind two molecules of ligand and one G protein". In fact, it was thought that G protein-coupled receptors were monomeric and that the stoichiometry between G protein-coupled receptors and G proteins was 1:1. From the subtitle, however, it is easily deduced that receptors occur as dimers and that the stoichiometry is one G protein for each dimer, i.e. for every two G protein-coupled receptors. Then the hypothesis is that there are two protomers forming the receptor dimer, each able to bind a molecule of ligand and the receptor dimer, interacting with only one G protein. Currently, this hypothesis is controversial in the G protein-coupled-receptor field.

The results indicate that co-expression of wild-type serotonin 5-HT2C receptor and a mutant 5-HT2C receptor, which is incapable of binding the ligand or stimulating inositol phosphate signalling, has no effect on ligand binding to wild-type 5-HT2C receptors, but inhibits basal and serotonin-stimulated signalling, as well as constitutive and serotonin-stimulated endocytosis of wild-type receptors.

By means of FRET experiments, it was shown that inactive 5-HT2C receptors inhibit wild-type 5-HT2C receptor function by forming non-functional heterodimers expressed on the plasma membrane. These results are consistent with a model in which one GPCR dimer binds two molecules of ligand and one G protein and indicate that dimerization is essential for 5-HT receptor function. Taking into account that functional G protein-coupled receptors are (at least) dimers and not monomers, this hypothesis is more attractive for many than the one suggesting that a receptor dimer would interact with two G proteins.

Competing interests: None declared

Franco R: "I found this article very interesting not only for the content but also for the..." Evaluation of: [Herrick-Davis K et al. Inhibition of serotonin 5-hydroxytryptamine2c receptor function through heterodimerization: receptor dimers bind two molecules of ligand and one G-protein. J Biol Chem. 2005 Dec 2; 280(48):40144-51; doi: 10.1074/jbc.M507396200]. Faculty of 1000, 05 Sep 2008. F1000.com/1120616#eval576831

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Franco R: 2008. F1000.com/1120616#eval576831

Faculty of 1000 evaluations, dissents and comments for [Herrick-Davis K et al. Inhibition of serotonin 5-hydroxytryptamine2c receptor function through heterodimerization: receptor dimers bind two molecules of ligand and one G-protein. J Biol Chem. 2005 Dec 2; 280(48):40144-51; doi: 10.1074/jbc.M507396200]. Faculty of 1000, 05 Sep 2008. F1000.com/1120616

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Faculty of 1000: 2008. F1000.com/1120616

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Although dimerization appears to be a common property of G-protein-coupled receptors (GPCRs), it remains unclear whether a GPCR dimer binds one or two molecules of ligand and whether ligand binding results in activation of one or two G-proteins when measured using functional assays in intact living cells. Previously, we demonstrated that serotonin 5-hydroxytryptamine2C (5-HT2C) receptors form homodimers (Herrick-Davis, K., Grinde, E., and Mazurkiewicz, J. (2004) Biochemistry 43, 13963-13971). In the present study, an inactive 5-HT(2C) receptor was created and coexpressed with wild-type 5-HT2C receptors to determine whether dimerization regulates receptor function and to determine the ligand/dimer/G-protein stoichiometry in living cells. Mutagenesis of Ser138 to Arg (S138R) produced a 5-HT2C receptor incapable of binding ligand or stimulating inositol phosphate (IP) signaling. Confocal fluorescence imaging revealed plasma membrane expression of yellow fluorescent protein-tagged S138R receptors. Expression of wild-type 5-HT2C receptors in an S138R-expressing stable cell line had no effect on ligand binding to wild-type 5-HT2C receptors, but inhibited basal and 5-HT-stimulated IP signaling as well as constitutive and 5-HT-stimulated endocytosis of wild-type 5-HT2C receptors. M1 muscarinic receptor activation of IP production was normal in the S138R-expressing cells. Heterodimerization of S138R with wild-type 5-HT2C receptors was visualized in living cells using confocal fluorescence resonance energy transfer (FRET). FRET was dependent on the donor/acceptor ratio and independent of the receptor expression level. Therefore, inactive 5-HT2C receptors inhibit wild-type 5-HT2C receptor function by forming nonfunctional heterodimers expressed on the plasma membrane. These results are consistent with a model in which one GPCR dimer binds two molecules of ligand and one G-protein and indicate that dimerization is essential for 5-HT receptor function.

DOI: 10.1074/jbc.M507396200

PMID: 16195233

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