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2017 Picower Lecture with Dr. Fred "Rusty" Gage
Monday, October 16 - 4:00 PM - 46-3002 (Singleton Auditorium)

Understanding what produces neuronal diversification has been a longstanding challenge for neuroscientists. At the heart of the search is the balance between genetics, inherited from both parents, and the environment that continuously shapes us through experiences. The recent finding that mobile elements such as retroelements are active in somatic neuronal progenitor cells provided an additional mechanism for neuronal diversification.

Retroelements are ancient mobile DNA found in most organisms. Long dismissed as selfish or “junk” DNA, they are thought to be intracellular parasites from our distant evolutionary past. Together with their mutated relatives, retrotransposons sequences constitute 45% of the mammalian genome and L1 elements alone, represent 20%. The fact that L1 can retrotranspose in a defined window of neuronal differentiation, changing the genetic information in single neurons in an arbitrary fashion, allows the brain to develop in distinctly different ways. This mechanism driving variety and diversity may contribute to the uniqueness of an individual brain.

However, the extent of the L1 impact in the neuronal genome is unknown. In this review, we will discuss the potential influence of L1 retrotransposition during brain development and the evolutionary clues that may have selected this unexpected machinery of diversity in neuronal precursor cells. We will also present preliminary data indicating environmental influence L1 activity in neuronal cells and that L1 retrotransposition frequency varies in a mental disorder syndrome genetic background. The characterization of somatic neuronal diversification will not only be relevant for the understanding of brain complexity and neuronal organization in mammals but might also shed light on the differences in cognitive abilities, personality traits and psychiatric conditions observed between humans.

Fred H. Gage, PhD, a Professor in the Laboratory of Genetics, joined The Salk Institute in 1995. He received his PhD in 1976 from The Johns Hopkins University. Dr. Gage's work concentrates on the adult central nervous system and unexpected plasticity and adaptability to environmental stimulation that remains throughout the life of all mammals. In addition, he models human neurological and psychiatric disease in vitro using human stem cells. Finally, his lab studies the genomic mosaicism that exists in the brain as a result of mobile elements that are active during neurogenesis.

Prior to joining Salk, Dr. Gage was a Professor of Neuroscience at the University of California, San Diego. He is a Fellow of the American Association for the Advancement of Science, a Member of the National Academy of Sciences and the Institute of Medicine, and American Philosophical Society, a foreign member of the European Molecular Biology Organization and a Member of the American Academy of Arts and Sciences. Dr. Gage has served as President of the Society for Neuroscience in 2002, and past President for the International Society for Stem Cell Research 2012.

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