Vangl-dependent planar cell polarity signalling is not required for neural crest migration in mammals.
Bottom Line: 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.PCP mutations are thus unlikely to mediate NC-related birth defects in humans.
Affiliation: Newlife Birth Defects Research Centre, Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.Show MeSH
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Mentions: To test experimentally whether Vangl1 may compensate for Vangl2 disruption in NC migration, we bred mice doubly homozygous for Vangl1 and Vangl2 loss of function (Song et al., 2010). The pattern of Erbb3-positive NC cell migration was very similar at both E8.5 and E9.5 in normally developing controls (Vangl1gt/+;Vangl2Δ/+; Fig. 3A,C-E) and in doubly homozygous mutants (Vangl1gt/gt;Vangl2Δ/Δ; Fig. 3B,F-H), despite the entirely open neural tube in the latter embryos. We conclude that Vangl gene function is not required for mouse NC migration in vivo.Fig. 3.
Affiliation: Newlife Birth Defects Research Centre, Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.