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XB-ART-55921
Nat Commun January 1, 2019; 10 (1): 1518.

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

Bajanca F , Gouignard N , Colle C , Parsons M , Mayor R , Theveneau E .


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.

PubMed ID: 30944331
Article link: Nat Commun

Genes referenced: cadm1 cdc42 cry2 cxcl12 cxcr4 ddx59 ets1 fas fn1 nrp1 nrp2 pxn rac1 rhoa sema3a sema3f snai2 sox9 tiam1 twist1
GO keywords: cell migration
Antibodies: Pxn Ab5 Rac1 Ab4


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