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. Author manuscript; available in PMC: 2017 Oct 26.
Published in final edited form as: Nature. 2017 Apr 26;545(7652):108–111. doi: 10.1038/nature22078

Figure 4. Expanded polyQ tracts inhibit ataxin-3-beclin 1 interaction, decrease beclin 1 levels and impair starvation-induced autophagy.

Figure 4

a,b HeLa cells were transfected with indicated constructs for 24 h and immunoprecipitated for endogenous beclin 1. a, Cells treated for last 6 h with proteasome inhibitor (MG132 10 µM) were analysed for beclin 1 ubiquitination and for beclin 1-bound polyQ using anti-GFP antibody. b, Immunocomplexes were analysed for beclin 1-bound ataxin-3 using anti-FLAG antibody. Bound ataxin-3/beclin 1 ratio is presented. c-d, Brain samples from wild-type (WT) mice and Huntington’s disease (HD) transgenic mice were analysed for beclin 1 (c) and LC3-II (d). WT fed n=7, HD fed n=5, WT fasted n=7, HD fasted n=6, a.u arbitrary units. Extended statistical analysis in Supplementary Table 1. Two-way ANOVA with Bonferroni’s post-test. Representative blots in Extended Data Fig. 8e. e-g, Primary fibroblasts from healthy controls or patients with different polyQ diseases treated with bafA1, in full media or starved/HBSS analysed for LC3-II/actin ratio. Gel source data in Supplementary Fig. 1.