Abstract
The migration of individual cells relies on their capacity to evaluate differences across their bodies and to move either toward or against a chemoattractant or a chemorepellent signal respectively. However, the direction of collective migration is believed to depend on the internal organization of the cell cluster while the role of the external signal is limited to single out some cells in the cluster, conferring them with motility properties. Here we analyzed the role of Fibroblast Growth Factor (FGF) signaling in collective migration in the Drosophila trachea. While ligand-binding FGF receptor (FGFR) activity in a single cell can drive migration of a tracheal cluster, we show that activity from a constitutively activated FGFR cannot-an observation that contrasts with previously analyzed cases. Our results indicate that individual cells in the tracheal cluster can "read" differences in the distribution of FGFR activity and lead migration of the cluster accordingly. Thus, FGF can act as a chemoattractant rather than as a motogen in collective cell migration. This finding has many implications in both development and pathology.
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