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. Author manuscript; available in PMC: 2017 Jun 20.
Published in final edited form as: Dev Cell. 2016 Jun 20;37(6):558–570. doi: 10.1016/j.devcel.2016.05.015

Figure 6. Rescue of Npc1a-deficiency phenotypes by inhibition of TOR and activation of autophagy.

Figure 6

(A) Inhibition of TOR in PG cells by overexpression of TSC1/2 suppresses accumulation of lipid droplet due to Npc1a-RNAi. (B) Developmental timing of pupariation and (C) pupal size. Stimulation of autophagy by overexpression of Atg1/13 in the PG rescues the Npc1a loss-of-function phenotype, indicating that increased autophagic clearance is sufficient to overcome the block in cholesterol trafficking in Npc1a deficient cells. (D) A model for TOR and EcR mediated regulation of cholesterol trafficking mechanisms in the PG cells. Detailed description of genotypes is given in Supplemental Experimental Procedures. Error bars indicate SEM (***P<0.001). See also Figure S4.