Title: Transposable elements and evolution of the human brain
Abstract: During the last 30-40 million years the primate brain has expanded in size, ultimately resulting in a new level of cognitive functions in humans. However, the genetic alterations driving this evolutionary process are poorly understood. Transposable elements have entered our genome as mobile elements, causing major interspecies differences in the composition of the genome. As a consequence, a large portion of genetic information specific to primates and humans is stored in transposable elements. Therefore, transposons are a likely candidate to have mediated evolutionary processes, including those which resulted in the complexity of the human brain. In this talk I will present evidence demonstrating a role for transposable elements in the evolution of the human brain.
Bio: Johan Jakobsson, PhD, is a Professor of Neuroscience at Lund University and a core member of the Lund Stem Cell Center. He did his PhD in Lund, Sweden, focusing on development of gene therapy strategies for the brain. After this, he trained as a postdoc at the EPFL, Lausanne, Switzerland, in the lab of Prof. Didier Trono focusing on transposable elements. His research is focusing on epigenetic mechanisms in the brain. He investigates the role of microRNAs, long non-coding RNAs and endogenous retroelements in neural stem cells and in neurons. His lab uses in vivo mouse models as well as human stem cell culture models to understand how epigenetics contribute to brain function. In addition, Dr. Jakobsson’s research contributes to the understanding and treatment of several brain disorders such as neurodegenerative disorders, psychiatric disorders and brain cancer.
Title: The role of transposable elements in neurodegenerative disease
Abstract: Transposable Elements (TEs) are sequences in the human genome that have (or once had) the ability to mobilize from one location in the genome to another. Most TEs that currently exist in the human genome are fixed and unable to mobilize, but many of these sequences have some residual level of functionality. These residual functions might include: the ability to bind DNA- or RNA-binding factors and act as regulatory elements, the ability to generate RNA transcripts, and/or the ability to encode proteins. Because TEs are extremely abundant in the human genome, covering nearly 45% of the sequence space, active TEs can have a large, and often deleterious, impact on host cell function. In particular, multiple studies have now shown elevated TE expression in the affected tissues of patients with several types of neurodegenerative disease. These include amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), fronto-temproal dementia (FTD), and multiple sclerosis (MS). I will present work from my lab on the ALS-associated protein TDP-43, which aggregates in ALS patient tissues, and how TDP-43 dysfunction contributes to de-silencing of transposable elements.
Bio: Molly received her Ph.D. in Physics & Astronomy from Dartmouth College in 2003. She was a postdoctoral fellow in the lab of Victor Ambros, where she studied gene regulation by small RNAs. She now runs a mixed computational and experimental lab at Cold Spring Harbor Laboratory to expand her studies of RNA mediated gene regulation with a particular focus on neurodegenerative disease. For this work, she was named a 2014 Rita Allen Foundation Scholar, and received the Ben Barres Early Career Acceleration Award in 2019.