In vivo topology converts competition for cell-matrix adhesion into directional migration

Fernanda Bajanca; Nadège Gouignard; Charlotte Colle; Maddy Parsons; Roberto Mayor; Eric Theveneau

doi:10.1038/s41467-019-09548-5

In vivo topology converts competition for cell-matrix adhesion into directional migration

Fernanda Bajanca, Nadège Gouignard, Charlotte Colle, Maddy Parsons, Roberto Mayor, Eric Theveneau^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

34 Citations (Scopus)

Abstract

When migrating in vivo, cells are exposed to numerous conflicting signals: chemokines, repellents, extracellular matrix, growth factors. The roles of several of these molecules have been studied individually in vitro or in vivo, but we have yet to understand how cells integrate them. To start addressing this question, we used the cephalic neural crest as a model system and looked at the roles of its best examples of positive and negative signals: stromal-cell derived factor 1 (Sdf1/Cxcl12) and class3-Semaphorins. Here we show that Sdf1 and Sema3A antagonistically control cell-matrix adhesion via opposite effects on Rac1 activity at the single cell level. Directional migration at the population level emerges as a result of global Semaphorin-dependent confinement and broad activation of adhesion by Sdf1 in the context of a biased Fibronectin distribution. These results indicate that uneven in vivo topology renders the need for precise distribution of secreted signals mostly dispensable.

Original language	English
Article number	1518
Journal	Nature Communications
Volume	10
Issue number	1
DOIs	https://doi.org/10.1038/s41467-019-09548-5
Publication status	Published - 3 Apr 2019

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abstract = "When migrating in vivo, cells are exposed to numerous conflicting signals: chemokines, repellents, extracellular matrix, growth factors. The roles of several of these molecules have been studied individually in vitro or in vivo, but we have yet to understand how cells integrate them. To start addressing this question, we used the cephalic neural crest as a model system and looked at the roles of its best examples of positive and negative signals: stromal-cell derived factor 1 (Sdf1/Cxcl12) and class3-Semaphorins. Here we show that Sdf1 and Sema3A antagonistically control cell-matrix adhesion via opposite effects on Rac1 activity at the single cell level. Directional migration at the population level emerges as a result of global Semaphorin-dependent confinement and broad activation of adhesion by Sdf1 in the context of a biased Fibronectin distribution. These results indicate that uneven in vivo topology renders the need for precise distribution of secreted signals mostly dispensable.",

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AU - Bajanca, Fernanda

AU - Gouignard, Nadège

AU - Colle, Charlotte

AU - Parsons, Maddy

AU - Mayor, Roberto

AU - Theveneau, Eric

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In vivo topology converts competition for cell-matrix adhesion into directional migration

Abstract

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