Vangl-dependent planar cell polarity signalling is not required for neural crest migration in mammals | Zendy

Sophie E. Pryor | Zendy; Valentina Massa | Zendy; Dawn Savery | Zendy; Philipp Andre | Zendy; Yingzi Yang | Zendy; Nicholas D. E. Greene | Zendy; Andrew J. Copp | Zendy

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Vangl-dependent planar cell polarity signalling is not required for neural crest migration in mammals

Author(s) -

Sophie E. Pryor,

Valentina Massa,

Dawn Savery,

Philipp Andre,

Yingzi Yang,

Nicholas D. E. Greene,

Andrew J. Copp

Publication year - 2014

Publication title -

development

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.754

H-Index - 325

eISSN - 1477-9129

pISSN - 0950-1991

DOI - 10.1242/dev.111427

Subject(s) - biology , neural crest , neural tube , cell migration , microbiology and biotechnology , xenopus , zebrafish , cell polarity , downregulation and upregulation , neural fold , mutant , embryo , polarity (international relations) , neural plate , hox gene , convergent extension , morpholino , cell , genetics , gene , embryogenesis , gene expression , gastrulation

The role of planar cell polarity (PCP) signalling in neural crest (NC) development is unclear. The PCP dependence of NC cell migration has been reported in Xenopus and zebrafish, but NC migration has not been studied in mammalian PCP mutants. Vangl2(Lp/Lp) mouse embryos lack PCP signalling and undergo almost complete failure of neural tube closure. Here we show, however, that NC specification, migration and derivative formation occur normally in Vangl2(Lp/Lp) embryos. The gene family member Vangl1 was not expressed in NC nor ectopically expressed in Vangl2(Lp/Lp) embryos, and doubly homozygous Vangl1/Vangl2 mutants exhibited normal NC migration. Acute downregulation of Vangl2 in the NC lineage did not prevent NC migration. In vitro, Vangl2(Lp/Lp) neural tube explants generated emigrating NC cells, as in wild type. Hence, PCP signalling is not essential for NC migration in mammals, in contrast to its essential role in neural tube closure. PCP mutations are thus unlikely to mediate NC-related birth defects in humans.

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