Parkinson’s disease genesinteract with ATP7 to regulate copper distribution and availability in Drosophila melanogaster
Authors: Brooke Allen; Alysia Vrailas-Mortimer
Affiliation: Illinois State University
Keywords: a. stress responses; a. neural degeneration
Copper is an essential element for enzymes that catalyze oxygen-dependent reactions. When an organism is exposed to either excess copper or deprived of copper, this micronutrient becomes detrimental. A mechanism used to control copper distribution and availability involves the ATPase transporter, ATP7. This X-linked transmembrane protein is responsible for delivering copper into the lumen of the cell by utilizing both endocytic and exocytic mechanisms. Mutations in ATP7 have been shown to cause Menkes disease and Wilson’s disease, which both share the phenotype of neurodegeneration. These genetic disorders with ATP7 defects both lead to mechanisms of neurodegeneration that is likely shared with other, more common neurodegenerative diseases, such as Parkinson’s disease. A screening of possible candidate genes that interact with ATP7 was conducted by inhibiting Parkinson’s disease genes in a ATP7 loss of function or ATP7 overexpression background. We find that several of the Parkinson’s disease genes showed a genetic interaction with ATP7, indicating that the mechanisms of neurodegeneration caused by ATP7 mutations may be conserved in Parkinson’s disease. These interactions and their link to neurological disorders will further discussed.