Fig. 7. Ultrastructural defects in compound eyes lacking dVps16A. Electron micrographs show details of compound eyes from wild type (A,E), white¹¹¹⁸ (C,F) or ey-Gal4 and GMR-Gal4>dVps16A-RNAi flies (B,D,G). Lenses (L) and pseudocones (P) are indicated in A and B. Primary pigment cells (PPC) face the pseudocones and contain type I granules, which appear electron dense. The larger type II granules are predominant in secondary pigment cells (SPC); they appear translucent because their content of pigments were washed out during the embedding process (A). Both types of pigment granules are absent after dVps16A knockdown (B). Rhabdomeres (Rh) contain the phototransduction cascade and are composed of tightly packed microvilli (C). After dVps16A knockdown (D), most rhabdomeres are only detected as remnants (arrows in D) in degenerating photoreceptors cells full of vacuoles and autophagosomes. The inset in D shows an example of an autophagosome with an internal piece of rough endoplasmic reticulum. (E-G) Photoreceptor cells (R) of neighboring ommatidia are separated by a layer of pigment cells. In wild-type eyes (E), the width of pigment cells (arrows) between photoreceptor cells (R) is dominated by type II pigment granules. These granules are essentially absent in white¹¹¹⁸ mutant eyes (F) resulting in a thin layer of pigment cells (between the arrows in F). After dVps16A knockdown (G), pigment cells are full of vacuoles and autophagosomes resulting in expanded width of the pigment cell layer (indicated between the arrows in G). Photoreceptors (R) in panel G were recognized by the remnants of rhabdomeres outside the field shown. Scale bar: 2 µm in A and G, 1 µm in B-F, and 100 nm for the inset in D.