Abstract
Leucinerichrepeat kinase 2(LRRK2) is a multifunctional domain protein, which molecular weight is 285kD.There have been identified that many mutation cause familial Parkinson disease.LRRK2 gene mutations are the most common genetic cause of Parkinson’s disease. However, little is known about the biological function of LRRK2 gene. In m ystudy, I use Drosophila as an animal model; overexpression of LRRK2 can increase Drosophila lifespan and resistance to oxidative stress. For example expression by pan neuronal driver Elav can extend lifespan and oxidative stress caused by paraquat and rotenone. Using GMR specific Gal4 driver to expression PolyQ and LRRK2 simultaneously can ameliorate 41Q induce eye degeneration, but not for 63Q and 108Q longer PolyQ induce toxicity. Moreover, I use three apoptosis related gene to examine the rescue efficiency by expression LRRK2 gene. I found that LRRK2 can reverse grim caused eye degeneration and down-size fly eyes, but there is little effect on hid or reaper induced eye abnormality. Ubiquitous expression of LRRK2 extends Drosophila lifespan and increase oxidative stress resistance. Toexamine which tissue is responsible for resistance to oxidative stress, we use Ddc(dopa-decarboxylase) Gal4 driver and its subset neuron drivers TH(dopaminergic) and TPH(serotoninergic)neurons, unlike our expectations, there is no protection on TH drive LRRK2 neurons ;however there is partially protection at lower concentration of paraquat on TPH neurons. To summarize my research, there is lifespan extension in Drosophila and oxidative stress by overexpression LRRK2 gene, and protection from 41Q induced eye degeneration. Finally expressions of LRRK2 show reduce the ability to grim cause down size of fly eyes and eye degeneration.