| First Author | Matsuo M | Year | 2022 |
| Journal | Cell Rep | Volume | 39 |
| Issue | 8 | Pages | 110844 |
| PubMed ID | 35613591 | Mgi Jnum | J:325323 |
| Mgi Id | MGI:7284014 | Doi | 10.1016/j.celrep.2022.110844 |
| Citation | Matsuo M, et al. (2022) A light-induced small G-protein gem limits the circadian clock phase-shift magnitude by inhibiting voltage-dependent calcium channels. Cell Rep 39(8):110844 |
| abstractText | Calcium signaling is pivotal to the circadian clockwork in the suprachiasmatic nucleus (SCN), particularly in rhythm entrainment to environmental light-dark cycles. Here, we show that a small G-protein Gem, an endogenous inhibitor of high-voltage-activated voltage-dependent calcium channels (VDCCs), is rapidly induced by light in SCN neurons via the calcium (Ca(2+))-mediated CREB/CRE transcriptional pathway. Gem attenuates light-induced calcium signaling through its interaction with VDCCs. The phase-shift magnitude of locomotor activity rhythms by light, at night, increases in Gem-deficient (Gem(-/-)) mice. Similarly, in SCN slices from Gem(-/-) mice, depolarizing stimuli induce larger phase shifts of clock gene transcription rhythms that are normalized by the application of an L-type VDCC blocker, nifedipine. Voltage-clamp recordings from SCN neurons reveal that Ca(2+) currents through L-type channels increase in Gem(-/-) mice. Our findings suggest that transcriptionally activated Gem feeds back to suppress excessive light-evoked L-type VDCC activation, adjusting the light-induced phase-shift magnitude to an appropriate level in mammals. |
