Atg6/UVRAG/Vps34-Containing Lipid Kinase Complex Is Required for Receptor Downregulation through Endolysosomal Degradation and Epithelial Polarity during Drosophila Wing Development
Figure 5
Atg6 and Atg14 are required for autophagy in contrast to UVRAG. (a)–(d) Larval wing discs expressing RNAi with transgenic Myc along with the autophagy marker mCherry-Atg8 in the patched (ptc) domain using ptcGal4. (a) In controls the expression of Myc induces massive autophagy in the ptc domain. (b) Atg6 or (c) Atg14 RNAi inhibited Myc-induced autophagy as the pattern of mCherry-Atg8 became dispersed in the citoplasm, whereas (d) UVRAG RNAi did not alter the pattern of the autophagy marker. (e), (g), and (i) Pupal wings expressing RNAi constructs by enGal4, immunostained against the selective autophagic cargo protein p62. (e) Atg6 or (g) Atg14 RNAi resulted in the massive accumulation of p62 aggregates. (i) UVRAG RNAi cells did not accumulate p62 aggregates. (f), (h), and (j) Quantification of (e), (g), and (i), respectively. On box plots, bars show the data ranging between the upper and lower quartiles; median of the signal covered areas is indicated as a horizontal black line within the box. Whiskers plot the smallest and largest observations, while dots and asterisks indicate outliers. NS means and means . For details and exact values of statistical analyses, see Table S3. For genotypes, see Table S4. Scale bars represent 25 μm in (a)–(d) and 15 μm in (e), (g), and (i).
