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Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis
Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis
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Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis
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Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis
Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis

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Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis
Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis
Journal Article

Supracellular contraction at the rear of neural crest cell groups drives collective chemotaxis

2018
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Overview
Neural crest cells migrate far and wide through a vertebrate embryo during development. Shellard et al. used Xenopus and zebrafish embryos to study how these clumps of mesenchymal cells migrate (see the Perspective by Adameyko). Movement was powered by a supracellular actomyosin cable that contracted around the rear of the clump. Similar supracellular contractility at the front was inhibited by a chemotactic signal. The imbalance in forces caused cells to rearrange so that the whole clump would be propelled forward. Science , this issue p. 339 ; see also p. 290 A rear engine drives collective chemotaxis in migrating Xenopus and zebrafish embryonic stem cells. Collective cell chemotaxis, the directed migration of cell groups along gradients of soluble chemical cues, underlies various developmental and pathological processes. We use neural crest cells, a migratory embryonic stem cell population whose behavior has been likened to malignant invasion, to study collective chemotaxis in vivo. Studying Xenopus and zebrafish, we have shown that the neural crest exhibits a tensile actomyosin ring at the edge of the migratory cell group that contracts in a supracellular fashion. This contractility is polarized during collective cell chemotaxis: It is inhibited at the front but persists at the rear of the cell cluster. The differential contractility drives directed collective cell migration ex vivo and in vivo through the intercalation of rear cells. Thus, in neural crest cells, collective chemotaxis works by rear-wheel drive.