The prechordal plate (arrows) is posteriorly displaced and elongated in a Wnt11 mutant (left). Activating endocytosis (right) corrects the defects.


Wnt signaling keeps a group of migrating cells together, say Florian Ulrich, Michael Krieg, Carl-Philipp Heisenberg (Max Planck Institute, Dresden, Germany), and colleagues. Wnt achieves this by promoting the recycling of adhesion molecules.

Signaling via Wnt11 is needed during vertebrate gastrulation, when the group of cells that will form the axial mesendoderm migrate en masse to the animal pole. Heisenberg's group finds that these cells are uncoordinated and migrate in various directions in the absence of Wnt11.

The authors found that Wnt11 mutants adhered less tightly, both to each other and to matrix proteins. “The ability to cohere,” says Heisenberg, “allows cells to align their [migratory] processes better. Loose clusters can project processes in all sorts of directions. Coherent ones can only put processes where there aren't any cells in the way.”

Adhesion in these cells is mediated by E-cadherin, which the authors show is properly recycled only in the presence of Wnt. The activation of endocytosis corrected the migratory problems of Wnt11 mutants, whereas loss of endocytosis weakened cell adhesion strengths. Wnt might induce endocytosis via its known ability to activate actomyosin contraction.

Though more surface cadherin should result from a block in endocytosis, Heisenberg thinks the total amount is less important than its dynamicity. “For cells to form cohesive clusters,” he says, “they need to undergo a lot of junctional remodeling, which might be dependent on E-cadherin recycling.”


Ulrich, F., et al.
Dev. Cell.