Abstract:
Neuronal communication depends on efficient vesicle recycling to sustain neurotransmission. Using C. elegans genetics, my lab investigates the molecular mechanisms coordinating endocytic proteins at synapses. In this talk, I will present two unpublished studies revealing new principles of synaptic vesicle recycling. The first uncovers mutations that allow a key endocytic protein to function without its canonical partner, shifting our understanding from protein–protein interaction models toward membrane remodeling mechanisms. The second shows how the intrinsically disordered Assembly Domain of AP180 controls vesicle size and release fidelity, and how actin interactions ensure vesicle quality control. Together, these findings reveal fundamental mechanisms that maintain reliable synaptic communication and inform our understanding of neurological health and disease.

Bio:
Jihong Bai grew up on the campus of Tsinghua University and lived in Beijing for 26 years. He received his undergraduate degree from Beijing Agricultural University (now China Agricultural University), and a master degree from Tsinghua University. He later joined the Biophysics PhD Program at the University of Wisconsin-Madison. In Madison, he studied biophysical properties of synaptotagmin, which is a major calcium sensor for the release of neurotransmitters. After receiving his PhD, he moved to Boston and joined the laboratory of Joshua Kaplan at Harvard Medical School to study synapse remodeling and neuronal communication using the nematode C. elegans. He joined Fred Hutch Cancer Center and started his lab in the winter of 2011.