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. Author manuscript; available in PMC: 2013 Aug 23.
Published in final edited form as: Neuron. 2012 Aug 23;75(4):618–632. doi: 10.1016/j.neuron.2012.06.026

Figure 2. Genetic modification of mitochondrial dynamics influences tau toxicity.

Figure 2

MARF is overexpressed using a UAS-MARF transgene (MARF OE) or reduced with transgenic RNAi (MARF RNAi). DRP1 is overexpressed using a UAS-DRP1 transgene (DRP1 OE), or reduced with transgenic RNAi (DRP1 RNAi). Tau is expressed when indicated (tau). (A) Mitochondrial length in neurons is altered by DRP1 or MARF manipulation in transgenic flies. n = 6 per genotype. Control (ctrl) is elav-GAL4/+;UAS-mitoGFP/+. (B) Neuronal degeneration as assayed by TUNEL staining is modified by DRP1 or MARF manipulation. n = 6 per genotype. (C) Oxidative stress is evaluated by quantification of dihydroethidium (DHE) fluorescence in whole mount brains, and shows elevated levels in tau transgenic flies compared to control. Quantification of DHE fluorescence in brain shows modification following DRP1 or MARF manipulation. n = 3 per genotype. (D) Cell cycle activation as measured by PCNA immunostaining is modified by DRP1 and MARF manipulation. n = 6 per genotype. Asterisks indicate P < 0.01, one-way ANOVA with Student-Neuman-Keuls test. Control (ctrl) in (B–D) is elav-GAL4/+. See also Fig. S2.