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

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. © 2021 The Authors. Published by Elsevier Inc.

Citation

Masaki Oba, Koji Fukui, Kazunori Sango, Mari Suzuki. Dataset on the effect of Rubicon overexpression on polyglutamine-induced locomotor dysfunction in Drosophila. Data in brief. 2021 Aug;37:107222

PMID: 34189208

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