#BlackInCompBio Seminar Series: Chantell Evans, PhD (Duke)
Time & Location
About the Event
Chantell received a B.S. in Chemistry from Southern Illinois University and her Ph.D. in Molecular and Cellular Pharmacology from the University of Wisconsin - Madison. Her graduate thesis investigated Ca2+-regulated exocytosis using biochemistry and biophysics. She completed her postdoctoral training at the University of Pennsylvania where she used advanced microscopy and biochemical techniques to gain insight into the molecular mechanisms that regulate mitophagy in primary neurons. Chantell is an inaugural recipient of the Hanna Gray Fellowship from the Howard Hughes Medical Institute.
"Neurons are post-mitotic, highly-polarized cells that must survive the lifespan of a human. They rely heavily on mitochondria to support local energy demands at distant fusion sites. These demands are supported by the continuous replenishment and maintenance of mitochondria. The complex morphology of neurons poses a unique challenge to maintain the mitochondrial network. A single human neuron is estimated to have two million mitochondria, where many organelles are located in far-reaching axons. How does a neuron survey every mitochondrion to continuously sustain a healthy mitochondrial population for the lifetime of a human? Emerging evidence suggests that multiple levels of mitochondrial surveillance are required, ranging from focal removal of damaged proteins and lipids to full degradation of dysfunctional organelles.
The focus of the Evans lab is to mechanistically define these diverse mitochondrial quality control pathways, including mitochondrial fusion and fission events, mitochondrial derived vesicles, and mitophagy. Our goal is to understand how these pathways collaborate to regulate the mitochondrial network in healthy neurons and what goes wrong in neurodegenerative disease. We integrate advanced live-cell microscopy to visualize mitochondrial dynamics with biochemical techniques and proteomics to define the specificity of these mechanisms in primary neurons, iPSCs, and mouse models of disease."
- General Attendee$0$00$0