Drosophila FGFR/Htl signaling shapes embryonic glia to phagocytose apoptotic neurons

Glial phagocytosis of apoptotic neurons is crucial for development and proper function of the central nervous system. Relying on transmembrane receptors located on their protrusions, phagocytic glia recognize and engulf apoptotic debris. Like vertebrate microglia, Drosophila phagocytic glial cells form an elaborate network in the developing brain to reach and remove apoptotic neurons. However, the mechanisms controlling creation of the branched morphology of these glial cells critical for their phagocytic ability remain unknown. Here, we demonstrate that during early embryogenesis, the Drosophila fibroblast growth factor receptor (FGFR) Heartless (Htl) and its ligand Pyramus are essential in glial cells for the formation of glial extensions, the presence of which strongly affects glial phagocytosis of apoptotic neurons during later stages of embryonic development. Reduction in Htl pathway activity results in shorter lengths and lower complexity of glial branches, thereby disrupting the glial network. Our work thus illuminates the important role Htl signaling plays in glial subcellular morphogenesis and in establishing glial phagocytic ability.

Automated summary

Glial phagocytosis of apoptotic neurons is crucial for the development and function of the central nervous system. In Drosophila, the fibroblast growth factor receptor Heartless (Htl) and its ligand Pyramus play an essential role in the formation of glial extensions, which in turn affect the phagocytic ability of glial cells later on. Reduction in Htl pathway activity disrupts the branching morphology of glial cells, impairing their ability to engulf apoptotic neurons. This study highlights the importance of Htl signaling in glial subcellular morphogenesis and the establishment of glial phagocytic ability.