Drosophila Torsin Protein Regulates Motor Control and Stress Sensitivity and Forms a Complex with Fragile-X Mental Retardation Protein

We investigated unknown in vivo functions of Torsin by using Drosophila as a model. Downregulation of Drosophila Torsin (DTor) by DTor-specific inhibitory double-stranded RNA (RNAi) induced abnormal locomotor behavior and increased susceptibility to H2O2. In addition, altered expression of DTor sign...

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Veröffentlicht in:Neural plasticity. - 1998. - 2016(2016) vom: 09., Seite 6762086
1. Verfasser: Nguyen, Phuong (VerfasserIn)
Weitere Verfasser: Seo, Jong Bok, Ahn, Hyo-Min, Koh, Young Ho
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2016
Zugriff auf das übergeordnete Werk:Neural plasticity
Schlagworte:Journal Article Drosophila Proteins Molecular Chaperones TOR1A protein, human Fragile X Mental Retardation Protein 139135-51-6 target of rapamycin protein, Drosophila EC 2.7.1.- TOR Serine-Threonine Kinases EC 2.7.11.1
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520 |a We investigated unknown in vivo functions of Torsin by using Drosophila as a model. Downregulation of Drosophila Torsin (DTor) by DTor-specific inhibitory double-stranded RNA (RNAi) induced abnormal locomotor behavior and increased susceptibility to H2O2. In addition, altered expression of DTor significantly increased the numbers of synaptic boutons. One important biochemical consequence of DTor-RNAi expression in fly brains was upregulation of alcohol dehydrogenase (ADH). Altered expression of ADH has also been reported in Drosophila Fragile-X mental retardation protein (DFMRP) mutant flies. Interestingly, expression of DFMRP was altered in DTor mutant flies, and DTor and DFMRP were present in the same protein complexes. In addition, DTor and DFMRP immunoreactivities were partially colocalized in several cellular organelles in larval muscles. Furthermore, there were no significant differences between synaptic morphologies of dfmrp null mutants and dfmrp mutants expressing DTor-RNAi. Taken together, our evidences suggested that DTor and DFMRP might be present in the same signaling pathway regulating synaptic plasticity. In addition, we also found that human Torsin1A and human FMRP were present in the same protein complexes, suggesting that this phenomenon is evolutionarily conserved 
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700 1 |a Seo, Jong Bok  |e verfasserin  |4 aut 
700 1 |a Ahn, Hyo-Min  |e verfasserin  |4 aut 
700 1 |a Koh, Young Ho  |e verfasserin  |4 aut 
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