Erik Jorgensen

Biosketch

Erik Jorgensen is a geneticist studying the molecular mechanisms of synaptic transmission. He was born and raised in Saratoga, California. Jorgensen was a vocational arts student, draftsman and carpenter early on. Eventually, he graduated from the University of California at Berkeley in 1979. He studied centromere function in yeast with Sy Fogel at Berkeley, and then hepatitis proteins under Heinz Schaller at University of Heidelberg. He received his Ph.D. in 1989 from the Department of Genetics at the University of Washington, characterizing mutations in the Antennapedia locus in Drosophila with Richard Garber. Postdoctoral work was conducted in H. Robert Horvitz’s laboratory at MIT where he studied the genetic basis of GABA transmission in the nematode C. elegans. In 1994 Jorgensen established his own laboratory at the University of Utah. He is currently a Distinguished Professor in the School of Biological Sciences and an Adjunct Professor in the Departments of Human Genetics and Biomedical Engineering. In 2005, Jorgensen was named an Investigator of the Howard Hughes Medical Institute, and is a member of the National Academy of Sciences.

Research Interests

Erik Jorgensen is a geneticist studying the molecular mechanisms of synaptic transmission. The laboratory studies how synapses release neurotransmitter at enormous rates and at the same time replenishing vesicles under intense stimulation. Studies are typically initiated using the nematode C. elegans for forward genetics and findings validated in primary neuronal cultures. Characterization of mutant synapses includes electrophysiology, superresolution microscopy, and electron microscopy. The speed of fusion is maintained by docking synaptic vesicles near calcium channels, so that calcium reaches the fusion site within microseconds. Docking, priming and release probability is regulated by Unc13 proteins. Synaptic vesicle proteins and membrane must be recovered after fusing to the synaptic membrane. To capture images of endocytosis in a living organism, they combine optogenetics, high-pressure freezing and electron microscopy. Mouse neurons recycle membrane within 50 to 300 milliseconds after stimulation. This novel form of membrane recovery is called ultrafast endocytosis, and it allows the synapses to restore membrane tension as well as recover synaptic vesicle components to replenish the supply of synaptic vesicles.