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. 2011 May 4;31(18):6858–6870. doi: 10.1523/JNEUROSCI.0710-11.2011

Figure 2.

Figure 2.

MTM and its analogs SDK and SK are protective in a Drosophila melanogaster model of HD. A, MTM or its analogs SDK and SK significantly extend the lifespan of HD flies expressing exon 1 of Htt with 93 CAG repeats (Q93). The median survival of flies receiving no treatment was 9.5 d compared with 13 d for flies receiving 10 μm MTM or SDK in their food or 12 d for flies receiving 10 μm SK in their food. For the MTM and SDK feeding survival curves, p < 0.0001 was calculated by the Mantel–Cox and Gehan–Beslow–Wilcoxon tests, whereas for the SK feeding survival curves, p < 0.001 or p < 0.0005 were calculated by the Mantel–Cox and Gehan–Beslow–Wilcoxon tests, respectively. Feeding of PreB (10 μm) had no statistically significant effect on the survival of the HD flies. The median survival of these flies was 10 d. These results indicate that the DNA binding ability of MTM and its analogs is necessary for their protective effect in vivo. B, MTM and its analogs had no significant effect on mHtt transgene expression as measured by real-time PCR. This indicates that the protective effect of MTM, SDK, and SK is independent of modulation of mHtt levels in the flies. C, D, MTM (10 μm), SDK (10 μm), and SK (10 μm) feeding enhanced the number of rhabdomeres per ommatidium in HD flies compared with ones receiving no treatment. Rescue was calculated at 40, 45, and 81% compared with the control group by the formula 100 * (Rt − Rc)/7 − Rc, where Rc is the number of rhabdomeres per ommatidium in the control group, and Rt is the number of rhabdomeres per ommatidium in the treatment groups. PreB (10 μm) feeding did not ameliorate the loss of rhabdomeres per ommatidium observed in the HD Q93 flies, indicating that the DNA binding ability of MTM and its analogs is necessary to suppress the neurodegeneration observed in the eyes of the HD flies. ***p < 0.0001.