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Figure 2 | Molecular Neurodegeneration

Figure 2

From: Motor neuron apoptosis and neuromuscular junction perturbation are prominent features in a Drosophila model of Fus-mediated ALS

Figure 2

Expression of Fus/Caz in fly eyes leads to progressive eye defects in a dose- and age-dependent manner. (A) A wild-type eye showing the typical ommatidia structure. (B-I) Morphology of eyes expressing one or two copies of Fus, FusR521G, FusΔ32, or Caz by GMR-Gal4 at day 4 after adult hatching. Fus, FusR521G, and Caz expressing eyes exhibit ommatidia loss and necrotic lesions. (J) Retinal section of a wild-type fly eye stained with Eosin shows intact ommatidial and rhabdomere structure. (K-N) Retinal sections of eyes expressing two copies of Fus, FusR521G, FusΔ32, or Caz by GMR-Gal4 at 4 DAE were stained with Eosin. Rhabdomere structures were disintegrated and ommatidia were disorganized in eyes expressing Fus, FusR521G, or Caz, but not in eyes expressing FusΔ32. (O-R) Quantification of the eye defects when expressing the indicated constructs during aging. Eye defects were classified in three levels: 1, < 30% ommatidia loss; 2, 30-70% ommatidia loss, and 3, > 70% ommatidia loss. The percentages of flies with each level of eye defects are shown in different colors (1, green; 2, blue; 3, red). (S) Western blots were performed with eye extracts from flies in Figure 2O-R at the indicated time points to monitor the levels of protein expression. Each individual protein was expressed at the attP site of the 75B1 locus by GMR-Gal4 to ensure that the proteins were expressed at a comparable level.

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