Frizzled-9 impairs acetylcholine receptor clustering in skeletal muscle cells
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Fecha
2014-04
Profesor/a Guía
Facultad/escuela
Idioma
en
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Título del volumen
Editor
Frontiers Research Foundation
Nombre de Curso
Licencia CC
Atribution 4.0 International (CC BY 4.0)
Licencia CC
https://creativecommons.org/licenses/by/4.0/deed.es
Resumen
Cumulative evidence indicates that Wnt pathways play crucial and diverse roles to
assemble the neuromuscular junction (NMJ), a peripheral synapse characterized by the
clustering of acetylcholine receptors (AChR) on postsynaptic densities. The molecular
determinants of Wnt effects at the NMJ are still to be fully elucidated. We report here that
the Wnt receptor Frizzled-9 (Fzd9) is expressed in developing skeletal muscles during NMJ
synaptogenesis. In cultured myotubes, gain- and loss-of-function experiments revealed
that Fzd9-mediated signaling impairs the AChR-clustering activity of agrin, an organizer of
postsynaptic differentiation. Overexpression of Fzd9 induced the cytosolic accumulation
of β-catenin, a key regulator of Wnt signaling. Consistently, Fzd9 and β-catenin localize
in the postsynaptic domain of embryonic NMJs in vivo. Our findings represent the first
evidence pointing to a crucial role of a Fzd-mediated, β-catenin-dependent signaling on the
assembly of the vertebrate NMJ.
Notas
Indexación: Scopus.
Palabras clave
Frizzled Receptors, Wnt Proteins, Neuromuscular Junction, Acetylcholine Receptor, Postsynaptic, Skeletal Muscle
Citación
Frontiers in Cellular Neuroscience. Volume 8, Issue 1 APR. 17 April 2014. Article number 110
DOI
DOI: 10.3389/fncel.2014.00110