Our laboratory is interested in understanding how the diverse neuronal cell types are generated and maintained in the nervous system. We are taking a combined molecular, cellular, genetic, and genomic approach in the model organisms Drosophila and mouse. To study how neuronal diversity is generated, we focus on investigating the mechanisms of asymmetric division of neural stem cell that balances the self-renewal and differentiation potentials of neural stem cells. Of particular interest to us is the mechanism by which aberrant regulation of neural stem cell asymmetric division leads to brain tumor-like phenotypes. To study how neurons are properly maintained after they are integrated into neural networks, we are creating neurodegenerative phenotypes in Drosophila similar to that observed in Alzheimer's and Parkinson's diseases in humans. We are employing the power of fly genetics to identify genetic modifiers that can suppress or enhance these disease phenotypes. Given the unanticipated high level conservation of signaling pathways, regulatory mechanisms, and physiological processes between flies and mammals, our research promises to provide insights into fundamental mechanisms that control the generation and maintenance of neuronal diversity in humans.
My primary focus area is glioma stem cell therapeutics through the regulation of mitochondrial metabolism. I am currently interested in identifying molecular mechanisms of reverse electron transport and its therapeutic potential for targeting of glioma stem cell and other neurological disorders. In addition, I am investigating the translational potential of viral protein NSP1 in neurological disorders.
My work focuses on the genetic mechanism underlying mitochondrial pathology, neurodegeneration, and the role of ribosome-associated protein quality control in aging and age-related neurodegenerative diseases.