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

Pryor SE, Massa V, Savery D, Andre P, Yang Y, Greene ND, Copp AJ - Development (2014)

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.

View Article: PubMed Central - PubMed

Affiliation: Newlife Birth Defects Research Centre, Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.

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Normal NC migration in Vangl1/2 double mutants and after acute Vangl2 downregulation in the NC lineage. (A-H) Control (A,C-E; Vangl1gt/+; Vangl2Δ/+) and double-mutant (B,F-H; Vangl1gt/gt; Vangl2Δ/Δ) embryos exhibit normal migration of Erbb3-positive cranial NC (E8.5; A,B) and cranial/trunk NC (E9.5; C-H). Acute NC downregulation of Vangl2 to test for a possible compensatory mechanism in Vangl2Lp/Lp embryos (I) reveals identical YFP-positive NC migration in control (J-L; Vangl2+/flox; Wnt1-Cre) and downregulation (M-O; Vangl2Lp/flox; Wnt1-Cre) E9.5 embryos. Arrows indicate comparable streams of NC cells migrating from the trunk neural tube in both genotypes. Scale bars: 200 µm in A; 500 µm in C,F; 100 µm in J-O.
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DEV111427F3: Normal NC migration in Vangl1/2 double mutants and after acute Vangl2 downregulation in the NC lineage. (A-H) Control (A,C-E; Vangl1gt/+; Vangl2Δ/+) and double-mutant (B,F-H; Vangl1gt/gt; Vangl2Δ/Δ) embryos exhibit normal migration of Erbb3-positive cranial NC (E8.5; A,B) and cranial/trunk NC (E9.5; C-H). Acute NC downregulation of Vangl2 to test for a possible compensatory mechanism in Vangl2Lp/Lp embryos (I) reveals identical YFP-positive NC migration in control (J-L; Vangl2+/flox; Wnt1-Cre) and downregulation (M-O; Vangl2Lp/flox; Wnt1-Cre) E9.5 embryos. Arrows indicate comparable streams of NC cells migrating from the trunk neural tube in both genotypes. Scale bars: 200 µm in A; 500 µm in C,F; 100 µm in J-O.

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.


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

Pryor SE, Massa V, Savery D, Andre P, Yang Y, Greene ND, Copp AJ - Development (2014)

Normal NC migration in Vangl1/2 double mutants and after acute Vangl2 downregulation in the NC lineage. (A-H) Control (A,C-E; Vangl1gt/+; Vangl2Δ/+) and double-mutant (B,F-H; Vangl1gt/gt; Vangl2Δ/Δ) embryos exhibit normal migration of Erbb3-positive cranial NC (E8.5; A,B) and cranial/trunk NC (E9.5; C-H). Acute NC downregulation of Vangl2 to test for a possible compensatory mechanism in Vangl2Lp/Lp embryos (I) reveals identical YFP-positive NC migration in control (J-L; Vangl2+/flox; Wnt1-Cre) and downregulation (M-O; Vangl2Lp/flox; Wnt1-Cre) E9.5 embryos. Arrows indicate comparable streams of NC cells migrating from the trunk neural tube in both genotypes. Scale bars: 200 µm in A; 500 µm in C,F; 100 µm in J-O.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4197537&req=5

DEV111427F3: Normal NC migration in Vangl1/2 double mutants and after acute Vangl2 downregulation in the NC lineage. (A-H) Control (A,C-E; Vangl1gt/+; Vangl2Δ/+) and double-mutant (B,F-H; Vangl1gt/gt; Vangl2Δ/Δ) embryos exhibit normal migration of Erbb3-positive cranial NC (E8.5; A,B) and cranial/trunk NC (E9.5; C-H). Acute NC downregulation of Vangl2 to test for a possible compensatory mechanism in Vangl2Lp/Lp embryos (I) reveals identical YFP-positive NC migration in control (J-L; Vangl2+/flox; Wnt1-Cre) and downregulation (M-O; Vangl2Lp/flox; Wnt1-Cre) E9.5 embryos. Arrows indicate comparable streams of NC cells migrating from the trunk neural tube in both genotypes. Scale bars: 200 µm in A; 500 µm in C,F; 100 µm in J-O.
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.

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.

View Article: PubMed Central - PubMed

Affiliation: Newlife Birth Defects Research Centre, Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.

Show MeSH
Related in: MedlinePlus