Keynote Lecture
Lynne E. Maquat, PhD.
J. Lowell Orbison Endowed Chair and Professor of Biochemistry & Biophysics
Founding Director of the Center for RNA Biology
University of Rochester Medical Center
Lynne E. Maquat, PhD is the J. Lowell Orbison Endowed Chair and Professor of Biochemistry & Biophysics who
holds concomitant appointments in Pediatrics and in Oncology, Founding Director of the Center for RNA Biology, and Founding Chair of Graduate Women in Science at the University of Rochester, Rochester, NY. After obtaining
her PhD in Biochemistry from the University of Wisconsin-Madison and undertaking post-doctoral work at the McArdle Laboratory for Cancer Research, she joined Roswell Park Cancer Institute before moving to the University of Rochester Medical Center. Dr. Maquat’s research focuses on the molecular basis of human diseases, with particular interest in mechanisms of mRNA decay. Maquat discovered nonsense-mediated mRNA decay (NMD) in human diseases in 1981 and, subsequently, the exon-junction complex (EJC) and how the EJC marks mRNAs for a quality-control “pioneer” round of protein synthesis. She also discovered Staufen-mediated mRNA decay, which mechanistically competes with NMD and, by so doing, new roles for short interspersed elements and long non-coding RNAs. Additionally, she has defined a new mechanism by which microRNAs are degraded, thereby regulating mRNAs so as to promote the cell cycle. One of her current interests focuses on the development of therapeutics for diseases that she has shown manifest hyperactivated NMD, including the most common single gene cause of intellectual disability and autism, Fragile X Syndrome.
Shou-wei Ding, PhD.
Distinguished Professor & Plant Pathologist
Microbiology & Plant Pathology Department
University of California, Riverside
The research programs in my lab focus on the host immune responses to RNA viruses and viral counter-defense strategies. Viruses with an RNA genome exhibit distinct genetic and immunological properties from DNA viruses. Many important human diseases (e.g. Ebola, influenza, SARS, Dengue, West Nile and polio) are caused by RNA viruses and > 70% of plant viruses are RNA viruses. RNA viruses that infect plants and animals are remarkably similar in genome structure and replication strategies. We have been taking a comparative approach to investigate the immune responses of plants, insects, nematodes and mammals to RNA viruses. Studies from my lab and others have shown that RNA viruses are targeted in plants, invertebrates and mammals by a conserved form of antiviral immunity mediated by RNA interference (RNAi). In antiviral RNAi, virus-specific dsRNA replicative intermediates are recognized and processed into small interfering RNAs (siRNAs) to guide specific virus clearance by RNAi. As a result, successful virus infection requires suppression of the antiviral immunity by a distinct class of viral proteins known as viral suppressors of RNAi (VSRs).
Lin He, PhD.
Professor & Thomas and Stacey Siebel Distinguished Chair in Stem Cell Research
Dept. of Molecular & Cell Biology
University of California, Berkeley
Lin He is the Thomas and Stacey Siebel Distinguished Chair professor and a professor in MCB department. Lin He is also a Biohub investigator in Chan-Zuckerberg Initiative.
While proteins are the structural and functional unit of living cells, only ~2% of mammalian genome contains protein -coding elements. It is increasingly clear that the ~98% mammalian genome has no protein-coding capacity, yet generates numerous non-protein-coding elements that regulate key biological processes. The He lab aims to elucidate the biological functions and molecular regulation of non-coding elements in mammalian development and disease, including miRNAs, long ncRNAs and transposable elements. Using an interdisciplinary approach combining mouse genetics and genomics, comparative genomics, cell and molecular biology, the He lab has elucidated an intricate crosstalk among non-coding RNAs, transposons and protein coding genes at the heart of the molecular regulation of key biological processes.
In contrast to the 2% mammalian genome that encode protein genes, nearly 40% mammalian genome originates from transposons. Transposons are a class of foreign sequences that hijack the host cellular machineries to invade, integrate and spread into the host genome. Transposons are traditionally viewed as parasitic invaders, and the vast majority are inactivated via degenerative mutations or transcriptional silencing. While most transposons are detrimental or neutral for the host, a subset of transposons are domesticated, and are employed by the host genome for gene regulation, genome innovation and genome stability. The co-opted transposons could alter gene expression regulation, modify gene coding structure and provide new protein-coding elements, substantially expanding the gene regulatory modality and transcript diversity in the host genome. Using genetics, genomics, computational biology, cell and molecular biology, the He lab will will elucidate the roles of transposons in reproductive aging and early embryogenesis.
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Klemens Hertel, PhD.
Professor, & Chair
Microbiology & Molecular Genetics, School of Medicine
University of California, Irvine
The Hertel lab's research focuses on understanding the mechanisms that allow for the generation of alternative splicing patterns. Their long-term goals are to understand how these processes are regulated, to relate the basic mechanisms of splice-site recognition to biological processes and to identify strategies to manipulate the expression of splicing isoforms in disease genes. To achieve these goals, the Hertel lab use a wide variety of approaches that include biochemistry, genetics, deep sequencing and bioinformatics. They are an interdisciplinary team with expertise in molecular biology, computational biology and physical chemistry.
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Dean of the Life Sciences Division
Keith and Cecilia Terasaki Presidential Endowed Chair
Professor, Molecular, Cell, and Developmental Biology
University of California, Los Angeles
Tracy Johnson was appointed dean of life sciences in September 2020. She is holder of the Keith and Cecilia Terasaki Presidential Endowed Chair, and a professor of molecular, cell, and developmental biology. Johnson, who joined the UCLA faculty in 2013, is recognized for her scientific leadership and contributions to educational innovation. She is a Howard Hughes Medical Institute Professor and has served as associate dean for inclusive excellence in the division of life sciences since January 2015.
Prior to joining UCLA, she was a member of the UC San Diego biological sciences faculty and a Jane Coffin Childs postdoctoral research fellow at the California Institute of Technology. She earned her bachelor’s degree in biochemistry and cell biology at UC San Diego and her doctorate in biochemistry and molecular biology at UC Berkeley.
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Daniel Lim, MD, PhD.
Professor
Department of Neurological Surgery, Weill Institute for Neurosciences
University of California, San Francisco
The focus of Dr. Lim’s research is on neural stem cells and neurogenesis. He is particularly interested in the molecular biology of the population of neural stem cells found in the subventricular zone (SVZ). For neural
stem cells to make neurons, daughter cells need to express certain sets of genes while repressing others. The maintenance of such lineage-specific transcriptional programs is in part regulated by chromatin structure – the “packaged” state of DNA with histone proteins. Recently, Dr. Lim’s work has revealed that the chromatin remodeling factor called Mixed Lineage Leukemia-1 (MLL1) is essential for postnatal neural stem cells to make new neurons. Currently, his work focuses on the molecular mechanisms by which MLL1 specifies a transcriptional program instructive for neurogenesis.
The Lim Laboratory also studies long non-coding RNAs (lncRNAs), which transcripts under 200 nucleotides long, with no evidence of protein coding potential. It is becoming clear that lncRNAs can have critical biological functions and roles in human neurological disease. Many lncRNAs interact with chromatin regulators and appear to regulate their function. The Lim Lab recently identified Pnky, a novel lncRNA transcript that is a potent regulator of neural stem cells in the embryonic and postnatal brain. Dr. Lim continues to study the function of this lncRNA in vivo and the molecular mechanisms by which it regulates neurogenesis.
In the future, Dr. Lim hopes to define the genetic programs and molecular mechanisms that guide the formation of neurons and glia from SVZ neural stem cells, and translate these discoveries into cell-based and genetic therapies for human neurological diseases.
Amy Pasquinelli, PhD.
Professor
Department of Molecular Biology, School of Biological Sciences
University of California, San Diego
Amy Pasquinelli received her Ph.D in Biomolecular Chemistry from the University of Wisconsin-Madison and was a Helen Hay Whitney Postdoctoral Fellow in the Genetics Department at Harvard Medical School. Since joining the faculty in 2003, she has been named a Keck Distinguished Young Scholar in Medical Research, a Searle Scholar, a V Foundation for Cancer Research Scholar, an Emerald Foundation Scholar and a Rosalind Franklin Young Investigator.
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Kathrin Plath, PhD.
Professor
Biological Chemistry
University of California, Los Angeles
The Plath lab has made numerous ground-breaking contributions that have vast impacts on the scientific community. For example, the lab is leading the way in the discovery of mechanisms underlying X-chromosome inactivation by the long non-coding RNA Xist, from identifying how the RNA can target an entire chromosome to defining protein crowding as the mechanism of action by which few Xist molecules can silence the the 1000 genes along the entire X chromosome. The work of the Plath lab on Xist is showing how RNAs can build functional nuclear compartments. The Plath lab also pioneered the understanding of different modes on X-chromosome dosage compensation by XIST RNA in early human development and discovered an unexpected autosomal function for the RNA with implications for understanding the female bias of diseases. They have also uncovered key mechanisms underlying transcription factor-induced reprogramming of somatic cells to induced pluripotent stem cells that are providing a considerable impetus for understanding and rationally designing cell fate transition. The Plath lab is specifically focus on how cis-regulatory enhancer elements are selected and activated by transcription factors. The Plath lab is also dissecting how genetic variation controls enhancer function.
In addition to continuing the work on X-chromosome dosage compensation, lncRNA function, enhancers and gene regulation, the Plath lab is now also aiming to understand how nutrients that vary with diet can regulate stem cell states and cell fate decisions, particularly those during development, with the ultimate goal to define dietary alterations that enable more accurate models of differentiation in the culture dish or lead to new treatments of pregnancy complications and diseases. Plath lab members are also using embryonic stem cells, induced pluripotent stem cells and new embryo models to understand the gene regulatory networks underlying cellular specification during development and pathophysiologies.
Often, the lab develops new single cell genomics technologies and apply them to their diverse biological model systems. In collaboration with the Gomperts lab, they are, for instance, deciphering the difference between the healthy and disease lung at a mechanistic and omics level applying novel multi-comics approaches.
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