HEARTLESS ENCODES A FIBROBLAST GROWTH-FACTOR RECEPTOR (DFR1 DFGF-R2) INVOLVED IN THE DIRECTIONAL MIGRATION OF EARLY MESODERMAL CELLS IN THEDROSOPHILA EMBRYO/

After invagination of the mesodermal primordium in the gastrulating Dr osophila embyro, the internalized cells migrate in a dorsolateral dire ction along the overlying ectoderm. This movement generates a stereoty ped arrangement of mesodermal cells that is essential for their correc t patterning by later position-specific inductive signals. We now repo rt that proper mesodermal cell migration is dependent on the function of a fibroblast growth factor (FGF) receptor encoded by heartless (htl ). In htl mutant embryos, the mesoderm forms normally but fails to und ergo its usual dorsolateral migration. As a result, cardiac, visceral, and dorsal somatic muscle fates are not induced by Decapentaplegic (D pp), a transforming growth factor beta family member that is derived f rom the dorsal ectoderm. Visceral mesoderm can nevertheless be induced by Dpp in the absence of htl function. Ras1 is an important downstrea m effector of Htl signaling because an activated form of Ras1 partiall y rescues the htl mutant phenotype. The evolutionary conservation of h tl function is suggested by the strikingly similar mesodermal migratio n and patterning phenotypes associated with FGF receptor mutations in species as diverse as nematode and mouse. These studies establish that Htl signaling provides a vital connection between initial formation o f the embryonic mesoderm in Drosophila and subsequent cell-fate specif ication within this germ layer.