UAS regulatory sequences drive expression of a full-length, pathogenic form of Hsap\ATXN3 (has a polyglutamine repeat of 77-80 residues) with both a mutation that results in the protein being catalytically inactive (amino acid replacement C14A) and also a mutation in Ubiquitin-binding site 2 (UbS2) that mildly disrupts binding to Rad23 protein (amino acid replacement W87A).