Early onset torsion dystonia is caused by mutations in DYT1 gene in humans. The molecular and cellular etiology underlying this disorder is not still understood yet. Because vertebrates have more than 4 homologs in their genomes, it is very hard to elucidate the exact in vivo functions of Torsin1A. Instead, Drosophila has only one homolog named Torsin. To investigate the in vivo functions of Torsin, we generated and characterized transgenic flies expressing coding regions of Drosophial Torsin (DTor) cDNA or double stranded inhibitory DNA constructs (RNAi). The transgenic expression of DTor cDNA or RNAi in all tissue induced significant changes in DTor proteins levels as well as ability of motor controls. In addition, DTor over-expressing flies showed increased resistance to H2O2 or paraquat. In the future study, we will found how those phenotypes were accomplished by performing various experiments.