Professor
Glendale, AZ
My lab team’s overarching research goal is to elucidate mechanisms by which absence of the parkin protein causes a subset of human dopaminergic neurons to degenerate. Parkin loss-of-function Drosophila is a particularly useful model in this context because the fruit fly has a brain region that is evolutionarily and functionally homologous to the brain structure that undergoes degeneration in Parkinson’s disease patients. Parkin-null flies have selective degeneration in this region and subsequent motor deficits that are easily observed. We were the first to report deficits in a heterozygous parkin loss-of-function model. Using transgenic flies that facilitate visualization of mitochondria and autophagosomes in vulnerable fly neurons in vivo, we have reported significant differences in mitochondrial protein oxidation, morphology, and turnover in degenerating parkin-null fly neurons; these differences were not observed in similar but non-degenerating neurons. Our recent efforts have laid the foundation for additional cell-specific gene editing studies that will allow us to address our overarching research question. In a few short generations, we can continue to observe the effects of gene expression changes in a cell-type specific manner, and compare degenerating and non-degenerating cells.
Title
Professor
Campus
Glendale, AZ
College
College of Health Sciences - AZ
College of Veterinary Medicine
College of Graduate Studies - AZ
Department
Biomedical Sciences
Program
Biomedical Sciences (M.A.)
Biomedical Sciences (M.B.S.)
Clinical Psychology
Veterinary Medicine
Molecular Cell Biology
Pharmacology I
Neuroscience
Society for Neuroscience
