Cell
Volume 160, Issues 1–2, 15 January 2015, Pages 313-323
Journal home page for Cell

Article
Subcellular Trafficking of FGF Controls Tracheal Invasion of Drosophila Flight Muscle

https://doi.org/10.1016/j.cell.2014.11.043Get rights and content
Under an Elsevier user license
open archive

Highlights

  • Tracheoles grow into (“invade”) flight muscle T-tubules

  • FGF, a tracheal chemoattractant, and its receptor are required for invasion

  • FGF localization switches from muscle surface to T tubules at the time of invasion

  • The switch requires a T-tubule trafficking pathway similar to epithelial trafficking

Summary

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.

Cited by (0)