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Journal Article

Forces driving epithelial spreading in zebrafish gastrulation.

MPS-Authors
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Behrndt,  Martin
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Campinho,  Pedro
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons219507

Oswald,  Felix
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Roensch,  Julia
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons145692

Grill,  Stephan W.
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

/persons/resource/persons219231

Heisenberg,  Carl-Philipp
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Behrndt, M., Salbreux, G., Campinho, P., Hauschild, R., Oswald, F., Roensch, J., et al. (2012). Forces driving epithelial spreading in zebrafish gastrulation. Science (New York, N.Y.), 338(6104), 257-260.


Cite as: https://hdl.handle.net/21.11116/0000-0001-0826-C
Abstract
Contractile actomyosin rings drive various fundamental morphogenetic processes ranging from cytokinesis to wound healing. Actomyosin rings are generally thought to function by circumferential contraction. Here, we show that the spreading of the enveloping cell layer (EVL) over the yolk cell during zebrafish gastrulation is driven by a contractile actomyosin ring. In contrast to previous suggestions, we find that this ring functions not only by circumferential contraction but also by a flow-friction mechanism. This generates a pulling force through resistance against retrograde actomyosin flow. EVL spreading proceeds normally in situations where circumferential contraction is unproductive, indicating that the flow-friction mechanism is sufficient. Thus, actomyosin rings can function in epithelial morphogenesis through a combination of cable-constriction and flow-friction mechanisms.