Academic Journal

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

التفاصيل البيبلوغرافية
العنوان: Activation of rhodopsin gene transcription in cultured retinal precursors of chicken embryo: role of Ca 2+ signaling and hyperpolarization-activated cation channels
المؤلفون: Bernard, Marianne, Dejos, Camille, Bergès, Thierry, Régnacq, Matthieu, Voisin, Pierre
المساهمون: Signalisation et Transports Ioniques Membranaires (STIM Poitiers ), Université de Poitiers = University of Poitiers (UP)-Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS)
المصدر: ISSN: 0022-3042.
بيانات النشر: HAL CCSD
Wiley
سنة النشر: 2014
المجموعة: Université François-Rabelais de Tours: HAL
مصطلحات موضوعية: calcium channels, hyperpolarization‐activated channels, photoreceptor, retina, rhodopsin, transcription, MESH: Animals, MESH: Calcium Signaling / physiology, MESH: Rhodopsin / genetics, MESH: Stem Cells / metabolism, MESH: Transcription, Genetic / physiology, MESH: Cells, Cultured, MESH: Chick Embryo, MESH: Chickens, MESH: Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels / physiology, MESH: Retina / cytology, MESH: Retina / embryology, MESH: Retina / metabolism, MESH: Rhodopsin / biosynthesis, [SDV]Life Sciences [q-bio]
الوصف: International audience ; 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 Ca 2+ -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 Ca 2+ rather than cAMP. This was confirmed by the inhibitory effect of general and T-type selective Ca 2+ channel blockers. Oscillations in Ca 2+ 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 Ca 2+ -channels, activation of Ca 2+ /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 Ca 2+ -dependent mechanism whereby hyperpolarization-activated cyclic nucleotide-gated channels (HCN) activate T-type voltage-dependent Ca 2+ 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 ...
نوع الوثيقة: article in journal/newspaper
اللغة: English
Relation: info:eu-repo/semantics/altIdentifier/pmid/25244004; hal-03165645; https://hal.science/hal-03165645; https://hal.science/hal-03165645/document; https://hal.science/hal-03165645/file/Bernard%20et%20al%20%28JNC-2013-0852-R1%29%20abridged%20with%20figures.pdf; PUBMED: 25244004
DOI: 10.1111/jnc.12624
الاتاحة: https://hal.science/hal-03165645
https://hal.science/hal-03165645/document
https://hal.science/hal-03165645/file/Bernard%20et%20al%20%28JNC-2013-0852-R1%29%20abridged%20with%20figures.pdf
https://doi.org/10.1111/jnc.12624
Rights: info:eu-repo/semantics/OpenAccess
رقم الانضمام: edsbas.40CA4226
قاعدة البيانات: BASE