Modulation of Kv Channel Gating by Light-Controlled Membrane Thickness

Voltage-gated potassium (Kv) channels are e ssential for shaping action potentials and rely on anionic lipids for proper gating, yet the mechanistic basis of lipid–channel interactions remains unclear. Cryo-electron microscopy studies suggest that, in the down state, arginine residues of the voltage...

Full description

Saved in:
Bibliographic Details
Main Authors: Rohit Yadav, Juergen Pfeffermann, Nikolaus Goessweiner-Mohr, Toma Glasnov, Sergey A. Akimov, Peter Pohl
Format: Article
Language:English
Published: MDPI AG 2025-05-01
Series:Biomolecules
Subjects:
Online Access:https://www.mdpi.com/2218-273X/15/5/744
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Voltage-gated potassium (Kv) channels are e ssential for shaping action potentials and rely on anionic lipids for proper gating, yet the mechanistic basis of lipid–channel interactions remains unclear. Cryo-electron microscopy studies suggest that, in the down state, arginine residues of the voltage sensor draw lipid phosphates upward, leading to a local membrane thinning of ~5 Å—an effect absent in the open state. To test whether membrane thickness directly affects voltage sensor function, we reconstituted Kv channels from <i>Aeropyrum pernix</i> (KvAP) into planar lipid bilayers containing photoswitchable lipids. Upon blue light illumination, the membrane thickened, and KvAP activity increased; UV light reversed both effects. Our findings indicate that membrane thickening weakens the interaction between lipid phosphates and voltage-sensing arginines in the down state, lowering the energy barrier for the transition to the up state and thereby promoting channel opening. This non-genetic, membrane-mediated approach provides a new strategy to control ion channel activity using light and establishes a direct, reversible link between membrane mechanics and voltage sensing, with potential applications in the remote control of neuronal excitability.
ISSN:2218-273X