Angela Poole

Previous Degrees

B.S. Engineering & Applied Sciences, California Institute of Technology.

Research

Parkinson's Disease is the second most common neurological disorder in the United States. Loss-of-function mutations in parkin are a major cause of autosomal recessive juvenile parkinsonism, and mounting evidence implicates parkin in late-onset and sporadic PD. We are conducting our studies of parkin in Drosophila melanogaster because of the powerful array of molecular and genetic tools available in this organism and because previous work indicates that neuronal developmental and functional properties and genetic pathways are conserved between fly and mammals.

Our previous work has shown that loss-of-function mutations in the Drosophila homolog of parkin result in spermatid formation defects, widespread apoptotic flight muscle degeneration, and degeneration of a subset of dopamine neurons in the central nervous system. Mitochondrial aberrations are a prominent and early feature of tissue degeneration in Drosophila parkin mutants, leading us to hypothesize that mitochondrial dysfunction is at the root of parkin mutant phenotypes. In an effort to link these phenotypes to the ubiquitin-protein ligase activity of Parkin, we are now using proteomic methods to I) Identify Parkin-binding components and II) Identify differentially ubiquitinated proteins in parkin mutants.

Bibliography

Poole, A. (2006). What does Parkin do? UW Genome Sciences Research Report. Seattle, WA.

Poole, A. (2006). Proteomic analysis of Parkin and PINK1. UW Genome Sciences Research Report. Seattle, University of Washington.

Poole, A. (2008). The PINK1/Parkin pathway influences mitochondrial morphology. UW Genome Sciences Research Report.

Poole, A., R. E. Thomas, et al. (2008). "The PINK1/Parkin pathway regulates mitochondrial morphology." Proceedings of the National Academy of Sciences 105(5): 1638-1643.