The non-canonical Wnt-PCP pathway shapes the caudal neural plate

The last stage of neural tube (NT) formation involves closure of the caudal neural plate (NP), an embryonic structure formed by neuromesodermal progenitors and newly differentiated cells that becomes incorporated into the NT. Here, we show in mouse that, as cell specification progresses, neuromesode...

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Detalles Bibliográficos
Autores: López-Escobar, Beatriz, Caro-Vega, J. M., Vijayraghavan, Deepthi S., Plageman, Timothy F., Sánchez-Alcázar, José Antonio, Moreno Martín Bejarano, Roberto Carlos, Savery, Dawn, Márquez-Rivas, Javier, Davidson, L. A., Ybot, Patricia
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2018
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/242510
Acceso en línea:http://hdl.handle.net/10261/242510
Access Level:acceso abierto
Palabra clave:Caudal neurulation
NMPs
NTDs
Wnt-PCP
Apical contraction
Tissue folding
Descripción
Sumario:The last stage of neural tube (NT) formation involves closure of the caudal neural plate (NP), an embryonic structure formed by neuromesodermal progenitors and newly differentiated cells that becomes incorporated into the NT. Here, we show in mouse that, as cell specification progresses, neuromesodermal progenitors and their progeny undergo significant changes in shape prior to their incorporation into the NT. The caudo-rostral progression towards differentiation is coupled to a gradual reliance on a unique combination of complex mechanisms that drive tissue folding, involving pulses of apical actomyosin contraction and planar polarised cell rearrangements, all of which are regulated by the Wnt-PCP pathway. Indeed, when this pathway is disrupted, either chemically or genetically, the polarisation and morphology of cells within the entire caudal NP is disturbed, producing delays in NT closure. The most severe disruptions of this pathway prevent caudal NT closure and result in spina bifida. In addition, a decrease in Vangl2 gene dosage also appears to promote more rapid progression towards a neural fate, but not the specification of more neural cells.