Expression of Vps16A^{dsRNA.Scer\UAS.WIZ} in posterior epidermal cells under the control of Scer\GAL4^5-56 prevents phagocytic clearance of ddaC neuron dendrite debris following pupal stage dendritic pruning. Similarly, when larval dendrites are injured (severed with an infrared laser) expression of Vps16A^{dsRNA.Scer\UAS.WIZ} under the control of Scer\GAL4^A58 blocks dendritic debris clearance.

Knock-down of Vps16A through expression of Vps16A^{dsRNA.Scer\UAS.WIZ} under the control of Scer\GAL4^da.G32 results in elevated levels of bacteria in primary hemocytes, suggesting an inability to digest them.

Dextran phagocytosed in LysoTracker experiments fails to reach lysosomes in flies expressing Vps16A^{dsRNA.Scer\UAS.WIZ} under the control of Scer\GAL4^da.G32 indicating lysosomal dysfunction rather than a defect in phagocytosis.

Expression of Vps16A^{dsRNA.Scer\UAS.WIZ} driven by Scer\GAL4^da.G32 leads to enlarged endosomes that are twice as big as those in wild-type.

Expression of Vps16A^{dsRNA.Scer\UAS.WIZ} under the simultaneous control of both Scer\GAL4^GMR.PF and Scer\GAL4^ey.PH results in a dramatic reduction of eye pigmentation compared to wild type. There is a gradient of pigmentation with the most anterior ommatidia having lost most of their pigmentation. The lenses overlaying each ommatidium appear correctly formed, but the pseudocones are essentially absent, with the remnants that are present being surrounded by a dense structure that is composed of vesicles and vacuolar structures containing internal vesicles. Type I pigment granules (normally found in primary pigment cells) and type II pigment granules (normally found in secondary pigment cells) are absent. The pigment cells are full of vacuoles and autophagosomes resulting in the pigment cell layer being expanded in width. Most photoreceptor cells contain only remnants of rhabdomeres, and the loss of rhabdomeres is accompanied by the accumulation of autophagosomes and vacuoles.