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. 2016 Nov 16;17:36. doi: 10.1186/s12860-016-0115-7

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — Defects in the endosomal pathway affect the distribution of the lysosomal hydrolase Cathepsin L. a-f Confocal sections of larval fat bodies with control clonal cells (a) or clonally expressing the dominant negative or silencing transgenes for Shibire (b), Rab5 (c), Rab4 (d), Chmp1 (e) or Rab7 (f). Fixed fat bodies were stained for the endogenous lysosomal hydrolase Cathepsin L. Clonal cells are outlined with a dotted line using the GFP-LAMP1 reporter also expressed by these cells as shown in the inset. Scale bar: 10 μm. g Quantification of the mean relative intensity of the Cathepsin L staining in transgene expressing cells compared to the staining intensity of 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-LAMP1/+; Ac > CD2 > Gal4/UAS-lucIR, b y w hs-FLP/UAS-ShiK44A; UAS-GFP- LAMP1/+; Ac > CD2 > Gal4/ UAS-ShiK44A, c y w hs-FLP/+; UAS-GFP-LAMP1/+; Ac > CD2 > Gal4/UAS-Rab5-IR, d y w hs-FLP/+; UAS-GFP-LAMP1/+; Ac > CD2 > Gal4/UAS-Rab4SN, e y w hs-FLP/+; UAS-GFP-LAMP1/+; Ac > CD2 > Gal4/UAS-Chmp1-IR, f y w hs-FLP/+; UAS-GFP-LAMP1/UAS-Rab7TN; Ac > CD2 > Gal4/+