Figures & data
Figure 1 Loss of the v0a1-dependent degradation pathway increases susceptibility to neurotoxic insults by human Aβ and tau proteins. (A) Representative ERG recording for at least n = 20 three day-old flies of the genotypes indicated and raised at room temperature under constant light stimulation. (B) Quantification of ERG depolarizations. Orange bar shows ERG depolarization for control or overexpressed proteins in wild type photoreceptors; blue bars are corresponding experiments with dicer2-enhanced v0a1 rNAi. Asterisks show statistical significance in pairwise comparisons (p < 0.005). (C) Immunolabeled adult eyes from experimental flies used for ERG recordings shown in (A). Chaoptin in green and nuclear labeling with Toto-3 in blue; Syx7/Avl labeling in red. Arrows indicate degenerative ‘holes’ in the immunolabeling. Arrowheads indicate early endosomal Syx7-positive accumulations with Chaoptin that are typical for loss of v0a1 function. Error bars are S.E.M.
Figure 2 v0a1 rNAi in photoreceptors causes phenotypes identical to loss of v0a1. (A–F) Antibody-labeling of Syx7/Avl and Sunglasses reveals similar accumulations of both markers in photoreceptors expressing dicer2-enhanced v0a1 RNAi (C and D) as in v0a1null mutant photoreceptors in ey35FLP v0a1 flies (E and F). (G) Both v0a1 RNAi as well as ey35FLP v0a1 lead to a complete loss of neurotransmission, as indicated by the loss of electroretinogram (ERG) ‘on’ transients.
