Subcellular trafficking of FGF controls tracheal invasion of Drosophila flight muscle

Cell. 2015 Jan 15;160(1-2):313-23. doi: 10.1016/j.cell.2014.11.043. Epub 2014 Dec 31.


To meet the extreme oxygen demand of insect flight muscle, tracheal (respiratory) tubes ramify not only on its surface, as in other tissues, but also within T-tubules and ultimately surrounding every mitochondrion. Although this remarkable physiological specialization has long been recognized, its cellular and molecular basis is unknown. Here, we show that Drosophila tracheoles invade flight muscle T-tubules through transient surface openings. Like other tracheal branching events, invasion requires the Branchless FGF pathway. However, localization of the FGF chemoattractant changes from all muscle membranes to T-tubules as invasion begins. Core regulators of epithelial basolateral membrane identity localize to T-tubules, and knockdown of AP-1γ, required for basolateral trafficking, redirects FGF from T-tubules to surface, increasing tracheal surface ramification and preventing invasion. We propose that tracheal invasion is controlled by an AP-1-dependent switch in FGF trafficking. Thus, subcellular targeting of a chemoattractant can direct outgrowth to specific domains, including inside the cell.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Membrane
  • Drosophila Proteins / metabolism
  • Drosophila melanogaster / growth & development*
  • Drosophila melanogaster / metabolism
  • Embryo, Nonmammalian / metabolism
  • Fibroblast Growth Factors / metabolism*
  • Larva / metabolism
  • Membrane Proteins / metabolism
  • Muscle Cells / cytology
  • Muscle, Skeletal / growth & development
  • Muscle, Skeletal / metabolism
  • Trachea / metabolism
  • Wings, Animal / embryology*


  • Drosophila Proteins
  • Membrane Proteins
  • Fibroblast Growth Factors