Harvard University COVID-19 updates

Department News

Thomas Südhof to Give 2023 JOHN M. Prather Lectures, April 12, 13, and 14

Thomas Südhof to Give 2023 JOHN M. Prather Lectures, April 12, 13, and 14

Thomas Südhof, one of the preeminent molecular and cellular neuroscientists in the world, will present the John M. Prather Lectures in Biology on April 12, 13, and 14, 2023.  A native of Germany, he completed medical and doctoral studies in Göttingen

He then moved to the University of Texas Southwestern Medical Center, where he was a postdoctoral fellow with Michael Brown and Joseph Goldstein, contributing to the analysis of cholesterol metabolism for which they won the Nobel Prize in 1985. He remained at UT Southwestern, joining the faculty and becoming an HHMI Investigator in 1986, and later chairing the Department of Neuroscience.  He moved to Stanford University in 2008, where he currently holds chairs in Cellular and Molecular Physiology, Psychiatry, and Neurology.

In his laboratory at UT Southwestern, Südhof began a comprehensive analysis of how neurotransmitters are released at synapses, the connections that neurons make with each other. He discovered and characterized many of the proteins responsible for this process, going on to probe their function in elegant biochemical, genetic and physiological studies. He shared the Nobel Prize for this work in 2013 with Randy Shekman and James Rothman.

At Stanford, Südhof has increasingly focused on a second, related theme: elucidating the mechanisms that underlie the specificity of synapse formation and determine synaptic properties.  He has identified a set of molecules that play key roles in these processes, leading to a deeper understanding of how neuronal circuits assemble during development and how they restructure throughout life.

Wednesday, April 12, 5:30 pm, Public Lecture, Science Center Hall B.  Towards a Neuronal Cell Biology of Alzheimer’s Disease

Major progress has been achieved recently in Alzheimer’s disease. New insights came in particular from human genetics, gene expression studies, and structural biology. These data suggest that Alzheimer’s disease develops as a result of the damage to neurons that is caused by pathological protein aggregation and that is exacerbated by an inappropriate or insufficient repair process mediated by immune cells called microglia and by astrocytes. However, how Alzheimer’s disease slowly develops over decades to impair brain functions and cause neuronal cell death remains enigmatic. In my talk, I will review the background of groundbreaking studies by others that provided the many insights into Alzheimer’s disease that are now emerging, and then discuss our own fledgling attempts to build on these insights and to contribute to a cell-biological understanding of how neurons are chronically impaired in the course of the disease.

Thursday, April 13, 12:00 pm, Seminar, Northwest Building B-103. Neurexins: Master Switches of Synapse Organization

Neurexins are presynaptic adhesion molecules that are expressed in thousands of splice variants and interact with more than 30 extracellular ligands, often in a manner regulated by alternative splicing. Data emerging over the last decade revealed a central role for neurexins in organizing synapse properties. Dependent on the neurexin isoform, its splice variant, and its ligands involved, neurexins control critical pre- and postsynaptic features that span almost all of synapse organization. Among these features are the presynaptic release probability, presynaptic neuromodulator responses, and postsynaptic glutamate receptor levels. Instead of trying to describe in my talk the entirety of these results, I will focus on two key projects that illustrate the central role of neurexins in synapses and provide an example for how these multifaceted proteins function as master switches of synapse properties.

Friday, April 14, 10:30 am, Seminar, Bio Labs Lecture Hall, 1080. Adhesion-GPCRs in Synapse Formation

In the last decade, two families of postsynaptic adhesion-GPCRs, latrophilins and BAI’s, have emerged as major drivers of synapse formation. However, how these adhesion-GPCRs orchestrate synapse assembly and other processes in brain remains unclear. Current data demonstrate that these adhesion-GPCRs interact with multiple ligands in synapse formation and function as true GPCRs, suggesting that synapse formation involves a classical signal transduction cascade pathway that is rendered specific for synapse assembly via defined extra- and intracellular interactions. In my talk, I will focus on recent results that illustrate facets of the function of these important molecules that constitute central regulators of how neural circuits are assembled and restructured continuously in brain.

by Josh Sanes

Thomas Südhof

Thomas Südhof