Figure 7. MiniCORVET promotes endosomal fusion upstream of HOPS.
Garland nephrocytes lacking the miniCORVET subunits Dor/Vps18 (B) or Vps16A (C) have fragmented Rab7-positive late endosomes compared to controls (A), whilst the early endosomal Rbsn-5 signal remains unchanged. In contrast, cells lacking Vps11 (D) or the HOPS specific subunit Lt/Vps41 (E) have enlarged Rab7-positive vesicles. (F) Double mutants for vps8 and lt display a phenotype similar to vps8 mutants, as Rab7-positive late endosomes appear as small dots filling the cytoplasm. (G) Quantification of data from panels (A–F). The median of data is indicated as a horizontal black line within the boxes. Bars show the upper and lower quartiles, ***p<0.001. Bars: 10 µm. Please see Figure 7—figure supplement 1. for additional data.
Figure 7—figure supplement 1. Additional miniCORVET and HOPS mutant nephrocyte data.
(A–C) Garland cells stained with anti-Rbsn-5 and Rab7. Knockdown of car (A) leads to fragmentation of late endosomes. In contrast, RNAi silencing of vps39 (B) or vps11 (C) results in the enlargement of late endosomes. Note that the phenotype of vps11 RNAi cells is identical to vps11 mutants shown in (Figure 7D. (D–L) Bars: 10 µm.