Rab2^Δ1 homozygous mutant larvae exhibit trafficking defects in the brain, ventral nerve cord, fat body, salivary glands, Garland cells and eye disc. E.g. in the brain, the lysosomal marker Lamp mislocalizes to cytoplasmic granules. In the salivary gland, the lysosomal marker Lamp mislocalizes to vesicles instead of showing the normal localization to a Lysotracker-positive tubulo-vesicular lysosomal network, and the lysosomal network seems fragmented. In the fat body, the lysosomal marker Lamp shows some mislocalization to vesicles instead of showing the normal localization to large, Lysotracker-positive autolysosomes, which are much smaller than in controls. In the eye discs there is a severe decrease in autophagy (i.e. fusion of autophagosomes to late endosomes, assessed by the green:red fluorescence ratio of GFP-mCh-Atg8a). In the Garland cells there are enlarged vacuoles and postendocytic trafficking defects (e.g. endocytozed proteins fail to be efficiently incorporated into Rab7-positive late endosomes and into Lysotracker-positive autolysosomes). The ventral nerve cord accumulates enlarged Rab7-positive late endosomes, as compared to controls.

Rab2^Δ1 homozygous pharate adults do not show any obvious defect in eye coloration compared to controls.