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. 2020 Jul 14;9(7):615. doi: 10.3390/antiox9070615

Figure 2.

Figure 2

hTDP-43-induced degenerative motor neuron and loss of neuromuscular junction (NMJ) were suppressed by expressing GstO2. (a) Representation of NMJ boutons labeled with anti-HRP-FITC at muscle 6/7 of segment 3 and quantification of the total number of boutons. Compared with the elav-Gal4 control larvae, hTDP-43 overexpression resulted in a significant reduction in the number of boutons. In the larvae co-overexpressing hTDP-43 and GstO2, the number of synaptic boutons was restored to a number similar to that of in control larvae. The quantification of data shows a genetic interaction between hTDP-43 and GstO2 on the total number of boutons per muscle area on muscle 6/7 of A3. Statistical significance was determined using the unpaired Student t-test (*** p < 0.001, n > 20 for each genotypes). Error bars indicate SEM. (b) Representative leg axon bundles labeled with membrane-tethered red fluorescent proteins (mCD8-RFP) in motor neurons specific to the D42-Gal4 driver. The white box indicates the region used for axon images. The expression of hTDP-43 in the motor neurons of fly legs showed severe axon degeneration, denoted by white arrows. The density of mCD8 signals in the axon area of the adult fly femur (dotted box) was suppressed by GstO2 overexpression. The quantification was performed by ImageJ software and normalized to the value of the D42-Gal4 control flies. Statistical significance was determined using the unpaired Student t-test (*** p < 0.001, n > 10 for each genotypes). Error bars indicate SEM.