Fig. 5.

Defects in the endosomal pathway affect the degradation of the autophagy substrate Ref(2)P/p62. a-e Confocal sections of larval fat bodies clonally expressing the dominant negative or silencing transgenes for Shibire (a), Rab5 (b), Rab4 (c), Chmp1 (d) or Rab7 (e). Fixed fat bodies were stained for the endogenous Ref(2)P/p62 protein. Clonal cells are outlined with a dotted line using the GFP-Atg8a reporter also expressed by these cells as shown in the inset. Scale bar: 10 μm. f Quantification of the size of the Ref(2)P/p62 aggregates in transgene expressing cells compared to the adjacent wild-type neighboring cells. Bars denote mean ± s.d. Statistical significance was determined using one-way ANOVA: *p < 0.05, **p < 0.005, ***p < 0.0005, ****p < 0.0001. Genotypes: a y w hs-FLP/UAS-ShiK44A; UAS-GFP-Atg8a/+; Ac > CD2 > Gal4/ UAS-ShiK44A, b y w hs-FLP/+; UAS-GFP- Atg8a/+; Ac > CD2 > Gal4/UAS-Rab5-IR, c y w hs-FLP/+; UAS-GFP- Atg8a/+; Ac > CD2 > Gal4/UAS-Rab4SN, d y w hs-FLP/+; UAS-GFP- Atg8a/+; Ac > CD2 > Gal4/UAS-Chmp1-IR, e y w hs-FLP/+; UAS-GFP- Atg8a/UAS-Rab7TN; Ac > CD2 > Gal4/+