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E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow
E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow
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E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow
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E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow
E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow

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E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow
E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow
Journal Article

E-cadherin focuses protrusion formation at the front of migrating cells by impeding actin flow

2020
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Overview
The migration of many cell types relies on the formation of actomyosin-dependent protrusions called blebs, but the mechanisms responsible for focusing this kind of protrusive activity to the cell front are largely unknown. Here, we employ zebrafish primordial germ cells (PGCs) as a model to study the role of cell-cell adhesion in bleb-driven single-cell migration in vivo. Utilizing a range of genetic, reverse genetic and mathematical tools, we define a previously unknown role for E-cadherin in confining bleb-type protrusions to the leading edge of the cell. We show that E-cadherin-mediated frictional forces impede the backwards flow of actomyosin-rich structures that define the domain where protrusions are preferentially generated. In this way, E-cadherin confines the bleb-forming region to a restricted area at the cell front and reinforces the front-rear axis of migrating cells. Accordingly, when E-cadherin activity is reduced, the bleb-forming area expands, thus compromising the directional persistence of the cells. The arrival of migratory cells at their targets relies on following precise routes within tissues. Here the authors demonstrate that the cell adhesion molecule E-cadherin can control the path of cell migration by confining the site where bleb-type protrusions form within the cell front.