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Calfacilitin is a calcium channel modulator essential for initiation of neural plate development

Calcium fluxes have been implicated in the specification of the vertebrate embryonic nervous system for some time, but how these fluxes are regulated and how they relate to the rest of the neural induction cascade is unknown. Here we describe Calfacilitin, a transmembrane calcium channel facilitator...

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Detalles Bibliográficos
Autores principales: Papanayotou, Costis, De Almeida, Irene, Liao, Ping, Oliveira, Nidia M. M., Lu, Song-Qing, Kougioumtzidou, Eleni, Zhu, Lei, Shaw, Alex, Sheng, Guojun, Streit, Andrea, Yu, Dejie, Wah Soong, Tuck, Stern, Claudio D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Pub. Group 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674269/
https://www.ncbi.nlm.nih.gov/pubmed/23673622
http://dx.doi.org/10.1038/ncomms2864
Descripción
Sumario:Calcium fluxes have been implicated in the specification of the vertebrate embryonic nervous system for some time, but how these fluxes are regulated and how they relate to the rest of the neural induction cascade is unknown. Here we describe Calfacilitin, a transmembrane calcium channel facilitator that increases calcium flux by generating a larger window current and slowing inactivation of the L-type Ca(V)1.2 channel. Calfacilitin binds to this channel and is co-expressed with it in the embryo. Regulation of intracellular calcium by Calfacilitin is required for expression of the neural plate specifiers Geminin and Sox2 and for neural plate formation. Loss-of-function of Calfacilitin can be rescued by ionomycin, which increases intracellular calcium. Our results elucidate the role of calcium fluxes in early neural development and uncover a new factor in the modulation of calcium signalling.