Figure 4.

TAT-BIND Inhibited Eye Degeneration, Delayed the Onset of Climbing Defects, and Extended the Lifespan of UAS-(GGGGCC)₃₆ Flies

(A) TAT-BIND treatment inhibited the eye degeneration of UAS-(GGGGCC)₃₆ flies. The flies were treated with 100 μM TAT-BIND or TAT-BIND-S for the external eye assay. Images of 1-day-old adult flies were taken. Genotypes were w; GMR-GAL4/UAS-(GGGGCC)₃ and w; GMR-GAL4/UAS-(GGGGCC)₃₆. The experiments were repeated thrice, and at least 30 flies were captured for scoring. (B) Statistical analysis of the scar formation of (A). (C) TAT-BIND treatment rescued the climbing defect of UAS-(GGGGCC)₃₆ flies at 10 days post-eclosion (dpe). (D) TAT-BIND treatment extended the lifespan of UAS-(GGGGCC)₃₆ flies. (E) Area under curve (AUC) analysis of (D). For the climbing ability and lifespan assays, flies at 2 dpe were fed with food containing different drug combinations, including vehicle control (ethanol), mifepristone (RU486, 200 μM), RU486 (200 μM) plus TAT-BIND (50 μM), and RU486 (200 μM) plus TAT-BIND-S (50 μM). Transgene expression was induced with mifepristone (RU486, 200 μM). The climbing ability assay was repeated six times, and at least 90 flies per treatment were scored. The lifespan assay was repeated at least six times, and more than 100 flies per treatment were recorded. Genotypes used in (C)–(E) were w; UAS-(GGGGCC)₃/+; elav^GS-GAL4/+ and w; UAS-(GGGGCC)₃₆/+; elav^GS-GAL4/+. Data were expressed as mean ± SEM. **p < 0.01, ***p < 0.001, and ****p < 0.0001; NS, no significance.