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Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways

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Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways. / Spoida, Katharina; Eickelbeck, Dennis; Karapinar, Raziye; Eckhardt, Tobias; Mark, Melanie D; Jancke, Dirk; Ehinger, Benedikt Valerian; König, Peter; Dalkara, Deniz; Herlitze, Stefan; Masseck, Olivia A.

In: CURR BIOL, Vol. 26, No. 9, 09.05.2016, p. 1206-12.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Spoida, K, Eickelbeck, D, Karapinar, R, Eckhardt, T, Mark, MD, Jancke, D, Ehinger, BV, König, P, Dalkara, D, Herlitze, S & Masseck, OA 2016, 'Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways', CURR BIOL, vol. 26, no. 9, pp. 1206-12. https://doi.org/10.1016/j.cub.2016.03.007

APA

Spoida, K., Eickelbeck, D., Karapinar, R., Eckhardt, T., Mark, M. D., Jancke, D., Ehinger, B. V., König, P., Dalkara, D., Herlitze, S., & Masseck, O. A. (2016). Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways. CURR BIOL, 26(9), 1206-12. https://doi.org/10.1016/j.cub.2016.03.007

Vancouver

Spoida K, Eickelbeck D, Karapinar R, Eckhardt T, Mark MD, Jancke D et al. Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways. CURR BIOL. 2016 May 9;26(9):1206-12. https://doi.org/10.1016/j.cub.2016.03.007

Bibtex

@article{61a1b60ac2fe40acaf8dff6a601c82b3,
title = "Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways",
abstract = "G-protein-coupled receptors (GPCRs) represent the major protein family for cellular modulation in mammals. Therefore, various strategies have been developed to analyze the function of GPCRs involving pharmaco- and optogenetic approaches [1, 2]. However, a tool that combines precise control of the activation and deactivation of GPCR pathways and/or neuronal firing with limited phototoxicity is still missing. We compared the biophysical properties and optogenetic application of a human and a mouse melanopsin variant (hOpn4L and mOpn4L) on the control of Gi/o and Gq pathways in heterologous expression systems and mouse brain. We found that GPCR pathways can be switched on/off by blue/yellow light. The proteins differ in their kinetics and wavelength dependence to activate and deactivate G protein pathways. Whereas mOpn4L is maximally activated by very short light pulses, leading to sustained G protein activation, G protein responses of hOpn4L need longer light pulses to be activated and decline in amplitude. Based on the different biophysical properties, brief light activation of mOpn4L is sufficient to induce sustained neuronal firing in cerebellar Purkinje cells (PC), whereas brief light activation of hOpn4L induces AP firing, which declines in frequency over time. Most importantly, mOpn4L-induced sustained firing can be switched off by yellow light. Based on the biophysical properties, hOpn4L and mOpn4L represent the first GPCR optogenetic tools, which can be used to switch GPCR pathways/neuronal firing on an off with temporal precision and limited phototoxicity. We suggest to name these tools moMo and huMo for future optogenetic applications.",
keywords = "Journal Article",
author = "Katharina Spoida and Dennis Eickelbeck and Raziye Karapinar and Tobias Eckhardt and Mark, {Melanie D} and Dirk Jancke and Ehinger, {Benedikt Valerian} and Peter K{\"o}nig and Deniz Dalkara and Stefan Herlitze and Masseck, {Olivia A}",
note = "Copyright {\textcopyright} 2016 Elsevier Ltd. All rights reserved.",
year = "2016",
month = may,
day = "9",
doi = "10.1016/j.cub.2016.03.007",
language = "English",
volume = "26",
pages = "1206--12",
journal = "CURR BIOL",
issn = "0960-9822",
publisher = "Cell Press",
number = "9",

}

RIS

TY - JOUR

T1 - Melanopsin Variants as Intrinsic Optogenetic On and Off Switches for Transient versus Sustained Activation of G Protein Pathways

AU - Spoida, Katharina

AU - Eickelbeck, Dennis

AU - Karapinar, Raziye

AU - Eckhardt, Tobias

AU - Mark, Melanie D

AU - Jancke, Dirk

AU - Ehinger, Benedikt Valerian

AU - König, Peter

AU - Dalkara, Deniz

AU - Herlitze, Stefan

AU - Masseck, Olivia A

N1 - Copyright © 2016 Elsevier Ltd. All rights reserved.

PY - 2016/5/9

Y1 - 2016/5/9

N2 - G-protein-coupled receptors (GPCRs) represent the major protein family for cellular modulation in mammals. Therefore, various strategies have been developed to analyze the function of GPCRs involving pharmaco- and optogenetic approaches [1, 2]. However, a tool that combines precise control of the activation and deactivation of GPCR pathways and/or neuronal firing with limited phototoxicity is still missing. We compared the biophysical properties and optogenetic application of a human and a mouse melanopsin variant (hOpn4L and mOpn4L) on the control of Gi/o and Gq pathways in heterologous expression systems and mouse brain. We found that GPCR pathways can be switched on/off by blue/yellow light. The proteins differ in their kinetics and wavelength dependence to activate and deactivate G protein pathways. Whereas mOpn4L is maximally activated by very short light pulses, leading to sustained G protein activation, G protein responses of hOpn4L need longer light pulses to be activated and decline in amplitude. Based on the different biophysical properties, brief light activation of mOpn4L is sufficient to induce sustained neuronal firing in cerebellar Purkinje cells (PC), whereas brief light activation of hOpn4L induces AP firing, which declines in frequency over time. Most importantly, mOpn4L-induced sustained firing can be switched off by yellow light. Based on the biophysical properties, hOpn4L and mOpn4L represent the first GPCR optogenetic tools, which can be used to switch GPCR pathways/neuronal firing on an off with temporal precision and limited phototoxicity. We suggest to name these tools moMo and huMo for future optogenetic applications.

AB - G-protein-coupled receptors (GPCRs) represent the major protein family for cellular modulation in mammals. Therefore, various strategies have been developed to analyze the function of GPCRs involving pharmaco- and optogenetic approaches [1, 2]. However, a tool that combines precise control of the activation and deactivation of GPCR pathways and/or neuronal firing with limited phototoxicity is still missing. We compared the biophysical properties and optogenetic application of a human and a mouse melanopsin variant (hOpn4L and mOpn4L) on the control of Gi/o and Gq pathways in heterologous expression systems and mouse brain. We found that GPCR pathways can be switched on/off by blue/yellow light. The proteins differ in their kinetics and wavelength dependence to activate and deactivate G protein pathways. Whereas mOpn4L is maximally activated by very short light pulses, leading to sustained G protein activation, G protein responses of hOpn4L need longer light pulses to be activated and decline in amplitude. Based on the different biophysical properties, brief light activation of mOpn4L is sufficient to induce sustained neuronal firing in cerebellar Purkinje cells (PC), whereas brief light activation of hOpn4L induces AP firing, which declines in frequency over time. Most importantly, mOpn4L-induced sustained firing can be switched off by yellow light. Based on the biophysical properties, hOpn4L and mOpn4L represent the first GPCR optogenetic tools, which can be used to switch GPCR pathways/neuronal firing on an off with temporal precision and limited phototoxicity. We suggest to name these tools moMo and huMo for future optogenetic applications.

KW - Journal Article

U2 - 10.1016/j.cub.2016.03.007

DO - 10.1016/j.cub.2016.03.007

M3 - SCORING: Journal article

C2 - 27068418

VL - 26

SP - 1206

EP - 1212

JO - CURR BIOL

JF - CURR BIOL

SN - 0960-9822

IS - 9

ER -