Regulation of serotonin-2C receptor G-protein coupling by RNA editing

Colleen M. Burns, Hsin Chu, Susan M. Rueter, Linda K. Hutchinson, Hervé Canton, Elaine Sanders-Bush and Ronald B. Emeson
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Colleen M. Burns: Vanderbilt University School of Medicine
Hsin Chu: Vanderbilt University School of Medicine
Susan M. Rueter: Vanderbilt University School of Medicine
Linda K. Hutchinson: Vanderbilt University School of Medicine
Hervé Canton: Vanderbilt University School of Medicine
Elaine Sanders-Bush: Vanderbilt University School of Medicine
Ronald B. Emeson: Vanderbilt University School of Medicine

Nature, 1997, vol. 387, issue 6630, 303-308

Abstract: Abstract The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) elicits a wide array of physiological effects by binding to several receptor subtypes. The 5-HT2 family of receptors belongs to a large group of seven-transmembrane-spanning G-protein-coupled receptors and includes three receptor subtypes (5-HT2A, 5-HT2B and 5-HT2C) which are linked to phospholipase C, promoting the hydrolysis of membrane phospholipids and a subsequent increase in the intracellular levels of inositol phosphates and diacylglycerol1. Here we show that transcripts encoding the 2C subtype of serotonin receptor (5-HT2CR) undergo RNA editing events in which genomically encoded adenosine residues are converted to inosines by the action of double-stranded RNA adenosine deaminase(s). Sequence analysis of complementary DNA isolates from dissected brain regions have indicated the tissue-specific expression of seven major 5-HT2C receptor iso-forms encoded by eleven distinct RNA species. Editing of 5-HT2CR messenger RNAs alters the amino-acid coding potential of the predicted second intracellular loop of the receptor and can lead to a 10–15-fold reduction in the efficacy of the interaction between receptors and their G proteins. These observations indicate that RNA editing is a new mechanism for regulating serotonergic signal transduction and suggest that this post-transcriptional modification may be critical for modulating the different cellular functions that are mediated by other members of the G-protein-coupled receptor superfamily.

Date: 1997
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DOI: 10.1038/387303a0

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