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Fig. 5. Lack of ß_H prevents dominant-negative Rab5 disruption of the early endosome. All cells are from first-instar guts except (J-L), which are from second-instar guts. Staining is for Rab5 (A,D,G,J,M, green in merge) and V-ATPase (C,F,I,L,O, red in merge). (A-C) Wild-type CC co-stained for Rab5 and V-ATPase, showing co-localization (arrowhead). (D-F) karst mutant CC co-stained for Rab5 and V-ATPase. At this stage, Rab5 endosomes appear intact and V-ATPase co-labels as in wild type (arrowhead). (G-I) Expression of Rab5S43N in wild-type CCs virtually eliminates the Rab5 signal at V-ATPase-positive endosomes (e.g. arrowhead) and eliminates the typical particulate Rab5 pattern. (J-L) By the second instar, wild-type CCs expressing Rab5S43N show non-overlapping distributions of Rab5 and V-ATPase. Rab5 is invariably concentrated adjacent to the septate junctions near the pore (arrowhead), whereas the V-ATPase is often seen in multiple compartments, especially in the apical cytoplasm of interstitial cells (L, asterisks). (M-O) Expression of Rab5S43N in karst mutant CCs fails to reduce the Rab5 signal at V-ATPase-positive endosomes (e.g. arrowhead) and does not eliminate the typical particulate Rab5 staining pattern. Identical results are seen in second-instar guts that still contain V-ATPase-positive endosomes (complete data set is shown in Fig. S4, supplementary material), except as noted in (J-L) above. Bars, 20 µm.

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