Serotonin signals through ciliary 5-HT6 to control insulin secretion

Ciliary 5-HT6 in pancreatic islet beta cells augments insulin secretion, and its plasma-membrane pool cannot drive release when the primary cilium is absent.

• Why it matters: Serotonin’s basal role in islet glucagon control is known, but how beta cells receive serotonin signals and whether cilia-localized receptors shape insulin output is unclear.
• What they did: The study localized the Gs-coupled serotonin receptor 6 (5-HT6) to primary cilia and plasma membranes in islet cells, then used a transgenic beta-cell cilia-loss model plus cilia-specific perturbations that preserved cilium architecture.
• The result: 5-HT6-dependent insulin secretion required the primary cilium, establishing subcellular localization as a determinant of GPCR function and defining ciliary 5-HT6 signaling as a distinct insulin-modulating pathway.

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