Dataset on the effect of Rubicon overexpression on polyglutamine-induced locomotor dysfunction in Drosophila

• Published in: Data in brief Vol. 37; p. 107222
• Main Authors: Oba, Masaki, Fukui, Koji, Sango, Kazunori, Suzuki, Mari
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.08.2021; Elsevier
• Subjects: Autophagy; Data; Drosophila melanogaster; Machado–Joseph disease; Polyglutamine; Spinocerebellar ataxia 3; Spinocerebellar ataxia 3; Polyglutamine; Autophagy; Drosophila melanogaster; Machado–Joseph disease
• ISSN: 2352-3409; 2352-3409
• DOI: 10.1016/j.dib.2021.107222

The accumulation of pathogenic misfolded proteins is believed to be a common mechanism of generation of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and polyglutamine (polyQ) diseases. The autophagy–lysosome degradation system has been considered as a potential therapeutic target against these disorders, as it is able to degrade large protein aggregates. Previously, we focused on Rubicon, a negative regulator of autophagy, and demonstrated that knockdown of the Drosophila homolog of Rubicon (dRubicon) suppressed locomotor dysfunction in a fly model of polyQ disease. This suppression was associated with increased autophagic activity and a marked reduction in the number of polyQ inclusion bodies [1]. We generated transgenic fly lines expressing hemagglutinin-tagged dRubicon wild-type (WT) or dRubicon in which the RUN [after RPIP8 (RaP2 interacting protein 8), UNC-14 and NESCA (new molecule containing SH3 at the carboxyl-terminus)] domain was deleted (ΔRUN). We provide data regarding the effect of WT and ΔRUN dRubicon co-expression on polyQ-induced locomotor dysfunction in Drosophila.