I graduated from Florida State University with a PhD in Neuroscience in May of 2017 and joined the O’Connell lab shortly thereafter as postdoctoral associate. I am studying the neural circuits involved in the control of food intake in the context of obesity. In general, obesity occurs when homeostatic mechanisms that regulate food intake and energy expenditure become dysregulated due to excessive caloric intake and decreased activity. Glial cells are critical to the development, function and maintenance of neuronal circuits involved in food intake. In particular, astrocytes – the most abundantly expressed glial cells in the brain – are well-established in their role of providing crucial metabolic support to neurons. I am interested in delineating the mechanisms by which diet-induced obesity modulates astrocyte-dependent changes in neuronal activity and feeding behavior. To do this, I use in vivo Ca2+ imaging and chemogenetic techniques to simultaneously modulate and measure neuronal and astrocyte activity while the mice are performing food-seeking behaviors. Ultimately, these studies should provide crucial insights into the progression of obesity as well as changes that may occur in astrocyte activity in response to high-fat diet.
Florida State University
Adv: Dr. Yi Zhou
Florida State University
B.S., Biological Sciences
The Jackson Laboratory Postdoctoral Associate Adv: Dr. Kristen O'Connell 2017-present
The aggresome is a key cytoplasmic organelle for sequestration and clearance of toxic protein aggregates. Although loading misfolded proteins cargos to dynein motors has been recognized as an important step in the aggresome formation process, the molecular machinery that mediates the association of cargos with the dynein motor is poorly understood. Here, we report a new aggresome-targeting pathway that involves isoforms of 14-3-3, a family of conserved regulatory proteins. 14-3-3 interacts with both the dynein-intermediate chain (DIC) and an Hsp70 co-chaperone Bcl-2-associated athanogene 3 (BAG3), thereby recruiting chaperone-associated protein cargos to dynein motors for their transport to aggresomes. This molecular cascade entails functional dimerization of 14-3-3, which we show to be crucial for the formation of aggresomes in both yeast and mammalian cells. These results suggest that 14-3-3 functions as a molecular adaptor to promote aggresomal targeting of misfolded protein aggregates and may link such complexes to inclusion bodies observed in various neurodegenerative diseases.