Model to explain Apn-mediated larval tracheal tube growth.

(A) Top: In the wild type (WT) dorsal trunk, the apical membrane grows along the axial axis (thick red arrows) and pulls the apical extracellular matrix (aECM), until the aECM resistance (indicated by green arrows) balances the forces provoked by tube elongation [33]. Bottom: In WT tracheal cells, Crb (blue) is enriched at the apical membrane where it controls apical surface growth. Apn (green) in the apical membrane is responsible for Crb maintenance and therefore ensures tube elongation. Crb trafficking involves recycling by the retromer to either the trans-Golgi network (TGN; blue vesicles) or to the plasma membrane (red vesicles), or by Rab11, or its degradation in the lysosome. (B) Top: In the apn1 mutant dorsal trunk, the pulling forces of the apical membrane expansion are decreased due to decreased growth of the apical membrane (thin red arrows), whereas the forces mediated by the aECM are likely to remain unchanged, causing breakage of the tube. Bottom: In the absence of Apn, Crb is depleted from the apical surface due to increased endocytosis. Crb is trapped in enlarged, Vps35 (retromer)-positive vesicles. It fails to be recycled (as shown by the lack of colocalization with Rab11), but is also not degraded, pointing to a functional defect of the retromer.