Molecular mechanism of calcium inhibition in viral channelrhodopsins

Abstract Viral channelrhodopsins (VCR1s) are giant-virus-encoded light-gated channels permeable to monovalent and divalent cations, including Na + and Ca 2+ ions, and inhibited by millimolar Ca 2+ concentrations. Here, we combine X-ray crystallography, time-resolved UV-vis spectroscopy, and ATR-FTIR spectroscopy to investigate molecular mechanisms of ion permeation and Ca 2+ -dependent inhibition in OLPVR1. An atomic resolution structure of OLPVR1 obtained in the presence of 10 mM CaCl 2 and 900 mM NaCl reveals a transient intracellular Ca 2+ binding site near T87 and T88, close to the retinal cofactor. Upon photoactivation, this Ca 2+ ion prevents a key rearrangement of the intracellular gate required for ion translocation, namely the flip of E44, thereby disrupting ion conduction. Instead, illumination leads to the accumulation of Na + ions between E44, S208 and the carbonyl oxygen of retinal-binding residue K204. Our findings reveal the molecular basis of Ca 2+ -dependent inhibition in VCR1s and provide a foundation for engineering enhanced tools for calcium optogenetics.

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Publication Details

Journal
Nature Communications
Published
2026-09-16
DOI
https://doi.org/10.1038/s41467-026-77716-5
Primary Topic
Photoreceptor and optogenetics research
Type
article
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article

Molecular mechanism of calcium inhibition in viral channelrhodopsins

Dmitrii Zabelskii, Hideki Kandori, Valentin Gordeliy, Josef Wachtveitl et al.
Nature Communications
Photoreceptor and optogenetics research
article

Molecular mechanism of calcium inhibition in viral channelrhodopsins

Dmitrii Zabelskii, Hideki Kandori, Valentin Gordeliy, Josef Wachtveitl, Mako Aoyama, Mikihiro Shibata, Gerrit H. U. Lamm, Siarhei Bukhalovich, Sergey Bukhdruker, Alexander Kuzmin, Vsevolod V. Sudarev, Kota Katayama, Ernst Bamberg
article en

Abstract

Abstract Viral channelrhodopsins (VCR1s) are giant-virus-encoded light-gated channels permeable to monovalent and divalent cations, including Na + and Ca 2+ ions, and inhibited by millimolar Ca 2+ concentrations. Here, we combine X-ray crystallography, time-resolved UV-vis spectroscopy, and ATR-FTIR spectroscopy to investigate molecular mechanisms of ion permeation and Ca 2+ -dependent inhibition in OLPVR1. An atomic resolution structure of OLPVR1 obtained in the presence of 10 mM CaCl 2 and 900 mM NaCl reveals a transient intracellular Ca 2+ binding site near T87 and T88, close to the retinal cofactor. Upon photoactivation, this Ca 2+ ion prevents a key rearrangement of the intracellular gate required for ion translocation, namely the flip of E44, thereby disrupting ion conduction. Instead, illumination leads to the accumulation of Na + ions between E44, S208 and the carbonyl oxygen of retinal-binding residue K204. Our findings reveal the molecular basis of Ca 2+ -dependent inhibition in VCR1s and provide a foundation for engineering enhanced tools for calcium optogenetics.

Nature Communications
Kanazawa University (JP), Goethe University Frankfurt (DE), Centre National de la Recherche Scientifique (FR), Moscow Institute of Physics and Technology (RU), Nagoya Institute of Technology (JP), Commissariat à l'Énergie Atomique et aux Énergies Alternatives (FR), CEA Grenoble (FR), Life Science Institute (JP), Max Planck Institute of Biophysics (DE), Institut de Biologie Structurale (FR), Université Grenoble Alpes (FR), European X-Ray Free-Electron Laser (DE)
Clean water and sanitation
Openalex Percentile: Top 16%
Photoreceptor and optogenetics research
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