Activation of rhodopsin gene transcription in cultured retinal precursors of chicken embryo: role of Ca 2+ signaling and hyperpolarization-activated cation channels - CNRS - Centre national de la recherche scientifique Accéder directement au contenu
Article Dans Une Revue Journal of Neurochemistry Année : 2014

Activation of rhodopsin gene transcription in cultured retinal precursors of chicken embryo: role of Ca 2+ signaling and hyperpolarization-activated cation channels

Résumé

This study reports that the spontaneous 50-fold activation of rhodopsin gene transcription, observed in cultured retinal precursors from 13-day chicken embryo, relies on a Ca2+-dependent mechanism. Activation of a transiently transfected rhodopsin promoter (luciferase reporter) in these cells was inhibited (60%) by cotransfection of a dominant-negative form of the cAMP-responsive element-binding protein. Both rhodopsin promoter activity and rhodopsin mRNA accumulation were blocked by Ca2+/calmodulin-dependent kinase II inhibitors, but not by protein kinase A inhibitors, suggesting a role of Ca2+ rather than cAMP. This was confirmed by the inhibitory effect of general and T-type selective Ca2+ channel blockers. Oscillations in Ca2+ fluorescence (Fluo8) could be observed in 1/10 cells that activated the rhodopsin promoter (DsRed reporter). A robust and reversible inhibition of rhodopsin gene transcription by ZD7288 indicated a role of hyperpolarization-activated channels (HCN). Cellular localization and developmental expression of HCN1 were compatible with a role in the onset of rhodopsin gene transcription. Together, the data suggest that the spontaneous activation of rhodopsin gene transcription in cultured retinal precursors results from a signaling cascade that involves the pacemaker activity of HCN channels, the opening of voltage-gated Ca2+-channels, activation of Ca2+/calmodulin-dependent kinase II and phosphorylation of cAMP-responsive element-binding protein.
Rhodopsin gene expression in cultured retinal precursors from chicken embryo relies on a Ca2+-dependent mechanism whereby hyperpolarization-activated cyclic nucleotide-gated channels (HCN) activate T-type voltage-dependent Ca2+ channels (VDCC) through membrane depolarization, causing calmodulin-dependent kinase II (CaMKII) to phosphorylate the cAMP-responsive element-binding protein (CREB) and leading to activation of rhodopsin gene transcription. Photoreceptor localization and development of HCN1 channels suggest similar role in vivo.
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hal-03165645 , version 1 (24-01-2024)

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Marianne Bernard, Camille Dejos, Thierry Bergès, Matthieu Régnacq, Pierre Voisin. Activation of rhodopsin gene transcription in cultured retinal precursors of chicken embryo: role of Ca 2+ signaling and hyperpolarization-activated cation channels. Journal of Neurochemistry, 2014, 129 (1), pp.85-98. ⟨10.1111/jnc.12624⟩. ⟨hal-03165645⟩
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