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

Abstract

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 R PIP8 ( R a P 2 i nteracting p rotein 8 ), U NC-14 and N ESCA ( ne w molecule containing S H3 at the ca rboxyl-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 .

LC3-associated phagocytosis promotes glial degradation of axon debris after injury in Drosophila models

“…Rubicon in mammals serves as the lynchpin of LAP-specific late phagosome (LAPosome) formation; besides its role in stimulating Vps34 activity on the phagosome, it stabilizes the NOX2 complex that generates ROS on LAPosomes, facilitating LC3-II incorporation 55 , 56 . Little is known about the fly ortholog of Rubicon 57 , 58 , so we sought additional evidence for its involvement in glial debris phagocytosis. We created frameshift mutants of Rubicon ( Rubicon fs1 and Rubicon fs2 ) by introducing small indels into the Rubicon coding region using CRISPR-Cas9 (Fig.…”

“…Atg101 Δ6h was a kind gift of Wanzhong Ge (Institute of Genetics, Zhejiang University School of Medicine, Hangzhou, China) 84 . The UAS-WT dRubicon::HA stock was described earlier 57 , 58 and was contributed kindly by Mari Suzuki (Tokyo Metropolitan Institute of Medical Science, Japan). The repo-GeneSwitch line was a gift of Véronique Monnier (Université de Paris, BFA Unit of Functional and Adaptative Biology, UMR 8251).…”

LC3-associated phagocytosis promotes glial degradation of axon debris after injury

“…Rubicon in mammals serves as the lynchpin of LAPosome formation; besides its role in stimulating Vps34 activity towards the phagosome, it stabilizes the NOX2 complex that generates ROS on LAPosomes, facilitating LC3-II incorporation 51,52 . Little is known about the fly ortholog of Rubicon 53,54 . We thus sought additional evidence for the involvement of Rubicon in glial debris phagocytosis.…”

“…Atg101 D6h was a kind gift of Wanzhong Ge (Institute of Genetics, Zhejiang University School of Medicine, Hangzhou, China) 84 . The UAS-WT dRubicon::HA stock was described earlier 53,54 and was contributed kindly by Mari Suzuki (Tokyo Metropolitan Institute of Medical Science, Japan).…”

“…To obtain the UAS-Rubicon::mRFP1 transgene, a Gateway entry vector (kind gift of Mari Suzuki, Tokyo Metropolitan Institute of Medical Science, Japan) bearing the full length Drosophila Rubicon cDNA coding sequence (pENTR-WT dRubicon) 54 was recombined with pTWR from the Carnegie Drosophila Gateway Vector Collection (Murphy lab) in an LR Clonase reaction according to the manufacturer's protocol (Gateway LR Clonase II Enzyme Mix, ThermoFisher Scientific). Resulting clones were sequenced and used for Drosophila transgenesis in w 1118 background based on standard protocols for P-element transformation.…”