ArticleBMC biology2017
Optogenetic interrogation reveals separable G-protein-dependent and -independent signalling linking G-protein-coupled receptors to the circadian oscillator.
Article in BMC biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Sex-Specific Methylomic and Transcriptomic Responses of the Avian Pineal Gland to Unpredictable Illumination Patterns.Journal of pineal research · 2025Article
- Selective optogenetic inhibition of GαProceedings of the National Academy of Sciences of the United States of America · 2024Article
- A visual opsin from jellyfish enables precise temporal control of G protein signalling.Nature communications · 2023Article
- Selective optogenetic control of GNature communications · 2022Article
- Optogenetic Modulation of Ion Channels by Photoreceptive Proteins.Advances in experimental medicine and biology · 2021Review
- Convergent evolution of tertiary structure in rhodopsin visual proteins from vertebrates and box jellyfish.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A live cell assay of GPCR coupling allows identification of optogenetic tools for controlling Go and Gi signaling.BMC biology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEndogenous circadian oscillators distributed across the mammalian body are synchronised among themselves and with external time via a variety of signalling molecules, some of which interact with G-protein-coupled receptors (GPCRs). GPCRs can regulate cell physiology via pathways originating with heterotrimeric G-proteins or β-arrestins. We applied an optogenetic approach to determine the contribution of these two signalling modes on circadian phase.
resultsWe employed a photopigment (JellyOp) that activates Gαs signalling with better selectivity and higher sensitivity than available alternatives, and a point mutant of this pigment (F112A) biased towards β-arrestin signalling. When expressed in fibroblasts, both native JellyOp and the F112A arrestin-biased mutant drove light-dependent phase resetting in the circadian clock. Shifts induced by the two opsins differed in their circadian phase dependence and the degree to which they were associated with clock gene induction.
conclusionsOur data imply separable G-protein and arrestin inputs to the mammalian circadian clock and establish a pair of optogenetic tools suitable for manipulating Gαs- and β-arrestin-biased signalling in live cells.
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