In autophagy-competent cells, CCT5 silencing enhanced the aggregation of transiently expressed GFP-tagged ATXN3(Q84) in HeLa cells (ataxin 3 protein with an expanded polyglutamine tract which causes spinocerebellar ataxia type 3 (ref. 46)) (Fig. 7a,b; Supplementary Fig. 10a), or long polyalanine tract EGFP-A19 (Fig. 7c) in MEFs and increased the levels of the endogenous autophagy substrate p62 in HeLa cells, primary cortical neurons and MEFs (Supplementary Fig. 10b–d). The gene discussed is ATXN3; the disease is Spinocerebellar ataxia type 3.