Cell migration is an important process during development whereby cells are released at defined stages and positions and move along characteristic routes. Such migration events are tightly regulated by molecules. Of particular interest is the molecular nature of signals responsible for the release of the cells, for the maintenance of cellular motility, or for directed migration and target finding.
All skeletal muscle in the body is generated from precursor cells that derive from the somite, in particular from a somite derivative that is called the dermomyotome. On particular axial levels, the dermomyotome delaminates migrating muscle progenitor cells that move over large distances to the anlage of the limbs, tongue and diaphragm where they form skeletal muscle. Now, Elena Vasyutina (laboratory of Prof. Carmen Birchmeier) and colleagues have discovered that CXCR4 and Gab1 cooperate to control the development of migrating muscle progenitor cells, implicating for the first time a chemokine receptor, CXCR4, in the migration of these muscle progenitor cells. CXCR4 is expressed on migrating progenitor cells, whereas its ligand, SDF1( Cxcl12), is produced by two of the targets of migration, the tongue and the limbs. Migrating muscle progenitor cells are attracted towards exogenous sources of SDF1. In addition, the scientists have shown that CXCR4 and Gab1, a molecule that transmits signals of the tyrosine kinase receptor met, genetically interact and contribute to the ability of muscle progenitor cells to reach their targets correctly. Changes in the migratory behavior of these cells in CXCR4/Gab1 mutant mice cause result in the absence of muscle groups in the limbs and tongue. Their findings have recently been published in the journal Genes and Development (Genes and Development doi/10.1101/gad.346205).
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