FIGURE 2 | Suppression of ent2 and adoR decreased mHTT-induced cytotoxicity and mHTT aggregate formation. (A) Retinal pigment cell degeneration in mHTT-expressing adult females (gmr > Q93) with RNAi silencing Ado metabolic enzymes, transporters, adoR ( adoR heterozygous mutant background), and mHTT-expressing flies under adoR homozygous mutant background. Blue arrows indicate treated groups showing a significantly reduced loss of pigment. † Eye image of control homozygous adoR 1 mutant without htt expression. Detailed methodologies for sample collection and eye imaging are described in section “Materials and Methods.” (B) Representative confocal images of the brains of 10-day-old mHTT-expressing adult females (elav > Q93) with RNAi silencing Ado metabolic enzymes, transporters, and adoR . Neuronal cells were detected with anti-Elav; mHTT aggregates were detected with anti-HTT (MW8). (C) Level of mHTT aggregate formation was calculated by normalizing the area of mHTT signal to the area of Elav signal. Significance in mHTT aggregate levels was analyzed using a Mann–Whitney U -test; significant differences between control Q93 flies and each RNAi treatment group are labeled as follows: * P < 0.05; ** P < 0.01; N.S., not significant. Error bars are presented as mean ± SEM. The number (n) of examined brain images are shown below each bar.