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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: The Alzheimer susceptibility gene BIN1 induces isoform-dependent neurotoxicity through early endosome defects

Fig. 4

BIN1iso1-induced neurodegeneration is rescued by regulators of the intracellular trafficking. a Representative images of 15-day-old retina expressing BIN1iso1 or luciferase (as a control) and constructs modulating Rab5, Rab7 and Rab11 activities. b Western blot analysis of BIN1, GFP derivatives in the corresponding conditions showing that BIN1 is not decreased in the conditions in which photoreceptor neurons are rescued. *Non-specific band. c–g Quantification of the BIN1iso1-induced neurodegeneration upon respective modulation of the early endosome regulator Rab5 activity, the recycling endosome regulator Rab11 activity, the late endosome regulator Rab7 and Rab9 activities, the lysosomal ATPase activity and Appl/APP. At the bottom of the graph, upper numbers indicate the number of quantified eyes per condition and lower numbers indicate the mean number of ommatidia quantified per eye. Statistical analysis was performed using a Kruskal Wallis test (p = 0.003643 for Rab5, p = 6.169 × 10−06 for Rab5DN and Rab5CA, p = 0.0001721 for Rab5 mutant and knockdown, p = 0.003643 for Rab11, p = 0.03487 for Rab11DN and Rab11CA, p = 0.1408 for Rab7, p = 0.24 for Rab7DN and Rab7CA, p = 0.8959 for Rab9, p = 0.1394 for lysosomal ATPase subunit knockdown, p = 0.006947 for Appl/APP) followed by Mann Whitney comparison (*p < 0.05, **p < 0.01, ***p < 0.001)

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