Event Details:
Helen S. Bateup, PhD
Assistant Professor of Neurobiology
University of California, Berkeley
Abstract
Research in my lab broadly aims to understand the cellular and molecular basis of neurological and psychiatric disease. We have a particular interest in “mTORopathies”, which are developmental brain disorders caused by mutations in the mTOR signaling pathway that lead to epilepsy, intellectual disability, and autism. To elucidate disease mechanisms for these disorders, we use genetic mouse and human cellular models in combination with a variety of techniques spanning molecular to behavioral. Our goal is to generate a mechanistic understanding of how disease-associated mutations affect the cell biology and physiology of specific types of neurons, and how altered neuronal activity impacts circuit function and behavior. In addition, we are investigating the early developmental alterations that may contribute to mTOR-related disorders using genetically engineered and patient-derived human brain organoids.
Bio
Dr. Bateup graduated from the honors program at Penn State University in 2000 summa cum laude with a B.S. degree in Biobehavioral Health and minor in Neuroscience. She completed a one-year post-baccalaureate research fellowship at the NIH prior to joining the graduate program at Rockefeller University 2001. In 2007, Dr. Bateup received her Ph.D., completing her dissertation work with Dr. Paul Greengard in which she established novel genetic mouse models to determine the cell type-specific consequences of dopamine signaling on striatal function. From there she joined Dr. Bernardo Sabatini’s lab as a post-doctoral fellow at Harvard Medical School to study how TSC-mTOR signaling affects synaptic function and excitatory/inhibitory balance in the hippocampus. In 2013, Dr. Bateup started her lab at the University of California, Berkeley in the Department of Molecular and Cell Biology and became a member of the Helen Wills Neuroscience Institute. The goal of her research is to elucidate the cellular and molecular basis of neurodevelopmental disorders. To do this, her lab takes a multi-faceted approach incorporating molecular, biochemical, electrophysiological, and behavioral analyses in genetic mouse models. In addition, she is investigating the early developmental alterations that may contribute to neurodevelopmental disorders using genetically engineered and patient-derived human brain organoids
Related Papers
[1] John D. Blair, Dirk Hockemeyer1 and Helen S. Bateup. Genetically engineered human cortical spheroid models of tuberous sclerosis. Nature Medicine, Volume 24, October 2018, Pages 1568-1578 DOI: 10.1038/s41591-018-0139-y
[2] Katelyn N. Benthall, Stacie L. Ong, Helen S. Bateup. Corticostriatal Transmission Is Selectively Enhanced in Striatonigral Neurons with Postnatal Loss of Tsc. CellPress, Volume 23, June 2018, Pages 3197-3208. DOI: 10.1016/j.celrep.2018.05.037