Suneel Apte, M.B.B.S, Ph.D. | Cleveland Clinic

American Heart Association Allen Distinguished Investigatorundefined

"Forward and reverse degradomics of cardiovascular extracellular matrix"

Abstract: Extracellular matrix (ECM) surrounds all cells and modifies all signals received by cells. It is thus not purely mechanical and hardly a static entity. Its turnover by proteases is a key element in its regulation, yet little is known about the global landscape of ECM breakdown, or proteolysis. Suneel Apte, M.B.B.S., D. Phil, will investigate how ECM is broken down in the cardiovascular system, both the physiological breakdown that occurs during heart development, and excess breakdown which may contribute to vascular disease. Too much breakdown is harmful because it weakens tissue structure and cells may react inappropriately to it. Apte and his team will use protein mass spectrometry to study all the changes in the extracellular matrix of the heart and blood vessels in a high-throughput approach intended to define the entire landscape of proteolysis. In addition to yielding a fundamental understanding of the biology of extracellular matrix breakdown, the work may uncover new cardiovascular disease biomarkers, disease pathways and targets for drug development.

Bio: Suneel Apte has a staff appointment at the Cleveland Clinic. He graduated from medical school at Bombay University and trained at first in orthopedic surgery. During clinical training, he moved to the University of Oxford, where he was supported by a Rhodes Scholarship and obtained a D.Phil under the mentorship of John Kenwright, Ph.D. He subsequently undertook post-doctoral training with Bjorn Olsen, Ph.D., at Harvard Medical School. During this period, he made the decision to switch to a career as a full-time scientist. His training experiences resulted in a long-term commitment to investigating connective tissues and ECM at a fundamental level. His laboratory discovered and characterized several ECM-degrading proteases with widespread relevance to embryogenesis and human disease. He utilizes genetic, molecular, cellular and proteomic approaches to investigate proteolytic turnover of ECM in cellular phenotype regulation, mammalian embryogenesis and inherited and acquired disorders. He has served the ECM community as President of the American Society for Matrix Biology and Chair of the Gordon Research Conference on Matrix Metalloproteinases.


Regina Barzilay, Ph.D. | MIT Computer Science & Artificial Intelligence Laboratory

"Learning to discover novel antibiotics from vast chemical spaces"undefined

Bio: Regina Barzilay is a professor in the Department of Electrical Engineering and Computer Science and a member of the Computer Science and Artificial Intelligence Laboratory at the Massachusetts Institute of Technology. Her research interests are in natural language processing. Currently, Prof. Barzilay is focused on bringing the power of machine learning to oncology. In collaboration with physicians and her students, she is devising deep learning models that utilize imaging, free text, and structured data to identify trends that affect early diagnosis, treatment, and disease prevention. Prof. Barzilay is poised to play a leading role in creating new models that advance the capacity of computers to harness the power of human language data.

Regina Barzilay is a recipient of various awards including the MacArthur Fellowship, NSF Career Award, the MIT Technology Review TR-35 Award, Microsoft Faculty Fellowship and several Best Paper Awards in top NLP conferences. In 2017, she received a MacArthur fellowship, an ACL fellowship and an AAAI fellowship.

Prof. Barzilay received her MS and BS from Ben-Gurion University of the Negev. Regina Barzilay received her PhD in Computer Science from Columbia University, and spent a year as a postdoc at Cornell University.


Jason Buenrostro, Ph.D. | Broad Institute of MIT and Harvard

"Multi-modal Visualization of the Dynamic Epigenome"undefined

Abstract: Since the three-dimensional configuration of DNA is crucial to determining which genes are expressed in a given cell, Chen and Buenrostro will develop a set of technologies to directly visualize the architecture of the genome and sequence individual regulatory elements within cells. This fundamental new capability will enable researchers to understand how spatial organization of the genome is regulated, and to ask new questions about how changes in the epigenome lead to changes in both normal and disease cell types directly within tissues.

Bio: Jason Buenrostro is a Broad Institute Fellow and Harvard Society Junior Fellow. At the Broad Institute, the Buenrostro Lab is developing new methods for understanding gene regulation within complex human tissues. To do this, the lab is integrating approaches across molecular biology, microscopy and large-scale bioinformatics to reveal new insights into the regulatory diversity of single-cells within healthy and diseased tissues.

Dr. Buenrostro is best known for his graduate work developing ATAC-seq and single-cell ATAC-seq methods for profiling epigenomes within rare populations and single-cells. Dr. Buenrostro completed his doctoral work at Stanford University Department of Genetics and earned undergraduate degrees in General Engineering and Biology at Santa Clara University.


Fei Chen, Ph.D. | Broad Institute of MIT and Harvard

"Multi-modal Visualization of the Dynamic Epigenome"undefined

Abstract: Since the three-dimensional configuration of DNA is crucial to determining which genes are expressed in a given cell, Chen and Buenrostro will develop a set of technologies to directly visualize the architecture of the genome and sequence individual regulatory elements within cells. This fundamental new capability will enable researchers to understand how spatial organization of the genome is regulated, and to ask new questions about how changes in the epigenome lead to changes in both normal and disease cell types directly within tissues.

Bio: Fei Chen is a Principal Investigator and Broad Fellow at the Broad Institute. He leads a research group that is pioneering molecular and microscopy tools to uniquely illuminate biological pathways and function. These tools include novel methods to sequence nucleic acids in situ to understand the spatial organization of cell and tissues. A major focus of his work is to elucidate how the structural architecture of the genome is related to regulation and function in health and disease.

Before joining the Broad, his thesis work at the Massachusetts Institute of Technology included the co-invention of expansion microscopy, a breakthrough technique that allows for super-resolution imaging of biological samples with conventional light microscopes. He is the recipient of the National Science Foundation Graduate Research Fellowship, the MIT Viterbi and Poitras Fellowships, and was an Axline scholar at the California Institute of Technology.


Michael Elowitz, Ph.D. | Caltech & Allen Discovery Center at UW Medicine

Cell Lineage Tracingundefined

Abstract: Scientists have been asking questions about the ancestry and lineage of cells for over a century, but tracing the relationships between generations of cells has faced significant technical challenges. In the past several years, teams led by Jay Shendure, M.D., Ph.D., at the University of Washington, Michael Elowitz, Ph.D., and Long Cai, Ph.D., at Caltech and Alex Schier, Ph.D., at Harvard have created new technologies that take advantage of modern gene editing methods to effectively trace cells as they divide, move and differentiate throughout an organism’s development.

The Allen Discovery Center for Cell Lineage Tracing will use these new technologies and paradigms to develop lineage maps for the zebrafish and mouse – the first global maps of development in any vertebrate. They will also develop genomic systems to record the molecular events that regulate development. The Center’s other investigators are Carlos Lois, Ph.D., at Caltech and Marshall Horwitz, M.D., Ph.D., UW professor of Pathology, and Cole Trapnell, Ph.D., UW assistant professor of Genome Sciences. 

Bio: Michael Elowitz is a Howard Hughes Medical Institute Investigator and Professor of Biology and Biological Engineering, and Applied Physics at Caltech. Dr. Elowitz's laboratory has introduced synthetic biology approaches to build and understand genetic circuits in living cells and tissues. Elowitz developed the Repressilator, an artificial genetic clock that generates gene expression oscillations in individual E. coli cells, and since then has continued to design and build other synthetic genetic circuits for programming or rewiring cellular functions. His lab also showed that gene expression is intrinsically stochastic, or ‘noisy’, and revealed how this noise functions to enable a variety of cellular functions, from probabilistic differentiation to time-based regulation. Currently, Elowitz’s lab is bringing synthetic “build to understand” approaches along with dynamic, quantitative single-cell imaging, to the kinds of developmental genetic circuits that allow organisms to develop from fertilized eggs into complex multicellular organisms. In particular, his lab has focused on cell-cell communication, epigenetic memory and cell fate control processes. Most recently, in collaboration with Long Cai, his lab demonstrated a synthetic system called MEMOIR that allows cells to record their own histories in their genomes. Elowitz received his PhD in Physics from Princeton University, and did postdoctoral research at Rockefeller University. Honors include the HFSP Nakasone Award, MacArthur Fellowship, Presidential Early Career Award, Allen Distinguished Investigator Award, and election to the American Academy of Arts and Sciences.


Rusty Gage, Ph.D. | Salk Institute

AHA-Allen Initiative in Brain Health and Cognitive Impairment Team Leaderundefined

Abstract: Rusty Gage, Ph.D., neuroscience researcher and President of Salk leads an interdisciplinary group of professors at Salk that believe that Alzheimer’s disease and other age-related brain disorders are triggered not by a single event, but by a failure of complex interwoven biological systems in our body that start to break down as we age. Their research team has developed unique new ways to study aging and diseased human neurons using brain “organoids” and marmosets as a new primate model of cognitive aging. They will now use these models to pursue a comprehensive understanding of the biology of aging and age-related diseases in an eight-year project. Gage’s theory is that failure in any one of these systems, which are integral to every cell in our bodies, puts pressure on the other processes, eventually causing a domino-like crash that causes devastating brain disorders like Alzheimer’s. Understanding the multi-part network that keeps our brains healthy could highlight pathways for better treatments for these diseases. 

Bio: Rusty Gage is President of the Salk Institute, professor in the Laboratory of Genetics and holds the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases. The Gage laboratory concentrates on the adult central nervous system and unexpected plasticity and adaptability to environmental stimulation that remains throughout the life of all mammals. His work may lead to methods of replacing or enhancing brain and spinal cord tissues lost or damaged due to neurodegenerative disease or trauma. 

Dr. Gage’s lab showed that, contrary to accepted dogma, human beings are capable of growing new nerve cells throughout life. Small populations of immature nerve cells are found in the adult mammalian brain, a process called neurogenesis. Dr. Gage is working to understand how these cells can be induced to become mature functioning nerve cells in the adult brain and spinal cord. His lab showed that environmental enrichment and physical exercise can enhance the growth of new brain cells. They are studying the underlying cellular and molecular mechanisms that may be harnessed to repair the aged and damaged brain and spinal cord. 


Charles Gersbach, Ph.D. | Duke University

"Epigenome Editing Technologies for Cell Programming"undefined

Abstract: The brain comprises an incredible diversity of cell types that act together to govern many complex functions. Studying these cell types in isolation, and understanding the role of epigenetic regulation in brain tissues, poses many technical challenges. Gersbach will aim to develop new technology to allow researchers to induce any epigenetic state in any cell type or tissue, and as a first application, use this technology to generate specific cell types of neurons in order to study drug response, disease, and the impact of epigenetic regulation on learning and memory.

Bio: Charles A. Gersbach is the Rooney Family Associate Professor at Duke University in the Departments of Biomedical Engineering and Orthopaedic Surgery, an Investigator in the Duke Center for Genomic and Computational Biology, and Director of the Duke Center for Biomolecular and Tissue Engineering. He received a Bachelor’s degree in Chemical Engineering and PhD in Biomedical Engineering from the Georgia Institute of Technology and Emory University where he studied new methods for applying genetic engineering to regenerative medicine. He then completed postdoctoral training at The Scripps Research Institute where he worked to develop new genome engineering tools.  His current research interests are in developing new genome and epigenome editing technologies and applying them to understand how gene regulation contributes to development, regeneration, disease, and drug response. He is also applying these tools to gene therapy, synthetic biology, and biomolecular and cellular engineering.  Dr. Gersbach’s work has been recognized through awards including the NIH Director’s New Innovator Award, the NSF CAREER Award, the Outstanding New Investigator Award from the American Society of Gene and Cell Therapy, and induction as a Fellow of the American Institute for Medical and Biological Engineering.


Chenghua Gu, Ph.D. | Harvard Medical School

"Brain vasculature at the neuro-immune interface"undefined

Abstract: Recently, researchers have come to appreciate that our brains and our immune systems are intricately connected, and that the dialogue between these two complicated systems is integral to human health and brain disease. Chenghua Gu studies the brain’s blood supply system, an elaborate vascular network that closely interacts with both the immune system and the brain.  Each neuron in the brain is nestled right next to a blood vessel and completely depends on its support for survival and function. Since immune signals are carried in the blood stream, the brain vasculature sits right at the interface between the immune system and the brain. Gu and her laboratory team will study the communication between nervous and immune systems by examining the specialized cells that line the brains’ blood vessels, known as endothelial cells, and how they receive and transmit signals between the body’s immune system and the brain. She has developed new ways to isolate brain endothelial cells from distinct brain regions of mice and study which genes they turn on and off, cell by individual cell, when peripheral immune challenges are applied. 

Bio: Chenghua Gu is a professor of neurobiology at Harvard Medical School. Her laboratory studies the interactions between the vascular and the nervous systems, specifically how the blood-brain barrier (BBB) functions and how neural activity rapidly increases local blood flow to meet moment-to-moment changes in regional brain energy demand – a process called neurovascular coupling. Her laboratory recently demonstrated that inhibition of transcytosis is a major mechanism for the BBB function, a surprising finding in view of the nearly exclusive focus on tight junctions as the mechanism of BBB integrity. Her findings imply that the molecular pathways inhibiting transcytosis could be targeted to open the BBB and deliver drugs to the central nervous system. Her lab also discovered that neural activity not only regulates local  blood flow, but also influences the structure of vascular networks, revealing a novel mechanism to match brain energy supply to neural demand. In earlier studies, Dr. Gu’s lab contributed to the recognition that the same guidance cues are used for wiring both the nervous and vascular systems, and discovered basic principles governing the establishment of neurovascular congruency.

Dr. Gu received her Ph.D. at Cornell Medical School and did her postdoctoral training at Johns Hopkins University School of Medicine. Dr. Gu was awarded the Whitehall Foundation Award (2007), the Klingenstein Fellowship Award (2007), March of Dimes Foundation Award (2007),and the  Alfred P. Sloan Research Fellowship (2008). Dr. Gu is a winner of the National Institutes of Health Director’s Pioneer Award for highly innovative research (2014). She was awarded the Bernice Grafstein Lecture (2015) at Weill Cornell Medical College, a lecture established to highlight the work of early-mid career women neuroscientists who are making their mark in their respective field. Dr. Gu is a Howard Hughes Medical Institute (HHMI) Faculty Scholar.


Jeffrey Holmes, M.D., Ph.D. | University of Virginia

American Heart Association Allen Distinguished Investigatorundefined

"Information Storage and Retrieval in the Cardiac Extracellular Matrix"

Abstract: Jeffrey Holmes, M.D., Ph.D., will study how information is coded and stored in the extracellular matrix over the long term - many of these fibrous proteins accumulate changes that can persist in the matrix for years, unlike cells in the same region, which turn over much more frequently. Holmes and his team aim to understand how these proteins are deposited and modified, how frequently they turn over, how changes in the proteins influence neighboring cells and how aging influences the process overall. To do so, the team will use approaches and expertise from the fields of bioengineering, immunology, physiology and chemistry to capture an integrated picture of extracellular matrix dynamics in the heart.

Bio: Jeffrey Holmes is a Professor of Biomedical Engineering and Medicine and the founding Director of the Center for Engineering in Medicine at the University of Virginia. He obtained his B.S. in Biomedical Engineering from the Johns Hopkins University in 1989, his Ph.D. in Bioengineering from the University of California, San Diego in 1995, and his M.D. from the University of California, San Diego in 1998. His Cardiac Biomechanics Group studies the interactions between mechanics, function, and growth and remodeling in the heart, using a combination of computational and experimental models. His research has been funded by the National Institutes of Health, the National Science Foundation, the American Heart Association, the Whitaker Foundation, the Coulter Foundation, the Hartwell Foundation, and the Paul G. Allen Frontiers Group. Dr. Holmes was awarded the Y.C. Fung Young Investigator Award in 2005, an American Heart Association Established Investigator Award in 2006, and the Van C. Mow Medal in 2018. He is a Fellow of the American Heart Association, the American Institute for Medical and Biological Engineering (AIMBE), and the American Society of Mechanical Engineers. 


Steve Horvath, Ph.D. | University of California, Los Angeles

"Universal Epigenetic Aging Clock for Vertebrates"undefined

Abstract: Because aging is a leading risk factor for multiple chronic diseases, including cancer, cardiovascular disease and neurodegenerative disorders like Alzheimer’s and Parkinson’s, finding a way to slow the biological aging process could offer a powerful medical tool. Horvath has recently developed a way to measure the age of any human tissue by looking at a combination of chemical changes to the DNA. This “epigenetic clock” is highly correlated with chronological age across the entire lifespan and even predicts life expectancy. Horvath will seek to enhance the clock so that it becomes a universal measure of aging across different species. The resulting epigenetic clock could shed light on a broad range of scientific questions, including why animals have different lifespans, how the environment influences lifespan, and potential trajectories to cancer and immune disorders as well as uncovering possible therapies for slowing the aging process.

Bio: Dr. Steve Horvath is a Professor in the Departments of Human Genetics and Biostatistics at the University of California, Los Angeles. His research lies at the intersection of computational biology, genetics, epidemiology, and systems biology. He works on all aspects of biomarker development with a particular focus on genomic biomarkers of aging. He recently published an article that describes a highly accurate biomarker of aging known as epigenetic clock. Salient features of the epigenetic clock include its high accuracy and its applicability to a broad spectrum of tissues and cell types. Dr. Horvath's most recent work demonstrates that the epigenetic clock captures aspects of biological age.


Mukesh Jain, M.D. | University Hospitals Cleveland Medical Center

AHA-Allen Initiative in Brain Health and Cognitive Impairment Team Leaderundefined

Abstract: Mukesh K. Jain, M.D., a cardiologist at University Hospitals Cleveland Medical Center and Professor of Medicine at Case Western Reserve University School of Medicine, will lead a team of investigators from University Hospitals Cleveland Medical Center, Johns Hopkins University, and University of Pennsylvania in a four-year project to explore how red blood cells, the most abundant cells in our body, and the inner lining of small blood vessels called endothelium work together as a unit to drive brain health and age-related cognitive disease. This unit of blood cells and blood vessels controls the delivery of oxygen and nutrients to our brain every second we are alive. Jain and his team will examine how connections between the red blood cells, blood vessels and the brain are altered during aging and disease and will test whether new therapeutics can restore the proper connections. 

Bio: Dr. Jain is Chief Scientific Officer, University Hospitals Health System, Chief Research Officer, University Hospitals Harrington Heart & Vascular Institute; the Ellery Sedgwick Jr. Chair & Distinguished Scientist; and Vice Dean for Medical Sciences and Professor of Medicine, Case Western Reserve University School of Medicine.  

Dr. Jain is internationally recognized for studies that established a central role for a family of transcription factors termed Kruppel-like factors, or KLFs, in cardiovascular biology, innate immunity, and metabolism. He has translated this work into animals and humans and demonstrated that KLFs are viable targets for therapeutic gain.  

Dr. Jain’s academic contributions are recognized by numerous awards and honors, including election to the National Academy of Medicine, the American Society for Clinical Investigation, American Association of Physicians, and Association of University Cardiologists. He is the 2015 recipient of the Judah Folkman Award in Vascular Biology from North American Vascular Biology Organization. Dr. Jain is a member of the American Heart Association’s Advancement of Science and Basic Science Council, and the National Heart, Lung, and Blood Institute (NHLBI) Board of External Experts. He is recipient of numerous grants, including the NHLBI Outstanding Investigator Award and the American Heart Association’s Established Investigator Award. He is a past president of the American Society for Clinical Investigation. He is a gifted mentor with mentorship awards from Harvard Medical School and Case Western Reserve University/University Hospitals Health System.


Ralf Jungmann, Ph.D. | Max Planck Institute of Biochemistry and LMU Munich

"Systematic mapping of epigenetic marks to the 3D architecture of the human genome in single cells"undefined

Abstract: Ralf Junmann and Jan Ellenberg will take an interdisciplinary approach combining chemical biology and biophysics to develop a novel technology to use barcoded fluorescent proteins to “paint” DNA sequences with specific epigenetic marks, and super-resolution microscopy to visualize those painted sequences at the level of single genes. With this tool, they will be able to map the complete 3D architecture of the epigenome in single human cells, and analyze how the structure changes during gene activation and repression.


Baljit Khakh, Ph.D. | University of California, Los Angeles

"Unmasking and Exploiting Astrocyte Biology"undefined

Abstract: Baljit Khakh will lead a project delving into the biology of an unsung type of brain cell, the astrocyte. Although almost half our brains are made up of astrocytes, we know far less about what they are and how they work than we do about neurons, a far more well-studied type of brain cell — and yet these cells may be linked to Alzheimer’s and other neurodegenerative diseases. Khakh and his laboratory team have recently developed new tools to better study the astrocyte, including optical and genetic approaches to visualize and manipulate astrocytes in a mouse brain as the animal reacts to different parts of its environs. In their project, they will study the suite of genes each astrocyte turns on or off, cell by cell, in an attempt to dispel the myth that all astrocytes are created equal. They will ask how astrocytes influence nearby neuron activity using novel methods created in the Khakh lab. And finally, they will apply these concepts and tools to determine how astrocyte activity is altered in a mouse model of Alzheimer’s disease, which afflicts more than 3 million people every year in the U.S. alone. Khakh hopes his research project may identify new possible therapeutic targets for this devastating disease which currently has no cure. 

Bio: Dr. Khakh is a Professor of Physiology and Neurobiology at UCLA. His laboratory has made important breakthroughs related to astrocyte biology. By developing new tools for glial research, they have discovered new forms of dynamic astrocyte signaling, unmasked neural circuit-specific astrocyte diversity and determined how these long-overlooked cells contribute to, and in some cases drive, neurological and psychiatric phenotypes.

Dr. Khakh was previously a Group Leader at the MRC Laboratory of Molecular Biology in Cambridge (UK), a Wellcome Trust International Prize Traveling Research Fellow at the California Institute of Technology and a Glaxo-Wellcome Postdoctoral Fellow at the University of Bristol. He completed his graduate work at the University of Cambridge. Dr. Khakh has received several awards, including the Bill Bowman Travelling Lectureship, the EMBO Young Investigator Award, The American Physiological Society S&R Foundation Ryuji Ueno Award, the UCLA H.W. Magoun Distinguished Lectureship, and the NIH Director’s Pioneer Award.


Marc Kirschner, Ph.D. | Harvard Medical School

"Reverse Engineering of Biological Circuits Underlying Aging and Development"undefined

Abstract: Marc Kirschner’s lab is taking a large-picture, systematic approach to understanding the biology of early development and of aging, two processes that bookend our lives and the lives of all living creatures. Typically, development and aging are studied in separate research fields, but Kirschner aims to use systems biology and machine learning approaches to uncover the cellular circuitry that drive each and to better understand where they might overlap, using as a model the small crustacean Daphnia magna, also known as the water flea.

Bio: Marc Kirschner has made major contributions to several areas of fundamental biology: embryology, cell organization, cell cycle regulation, evolution, and systems biology. In embryology, Kirschner studied the molecular basis of timing of embryonic events in early development. He discovered the mid-blastula transition, in which embryos make an abrupt transition from compressed cell cycles with virtually no transcription to a slower, complex cell cycle with massive transcription. Studying a later stage of development, his laboratory characterized the first embryonic inducer, where Kirschner developed the use of dominant negative proteins. His work on the cytoskeleton involved important discoveries in microtubules, actin filaments and nuclear lamins. His laboratory discovered the dynamic instability of microtubules, the distinct mechanism and role of GTP in microtubule assembly, and the protein tau, which regulates microtubule polymerization and is a major causal component of certain neurodegenerative diseases. In the actin field, he characterized the regulation of two major actin polymerization machines, the N-WASP and WAVE complexes. His work on the cell cycle, principally using biochemical methods in frog egg extracts, was key to establishing the basic cyclin/cdk1-based autonomous oscillator at work in all eukaryotic cells. In the course of that work, he identified and purified the anaphase promoting complex and its associated E2 enzymes that regulate the degradation of mitotic proteins and showed that one of them, securin, acts to hold the sister chromosomes together. In the course of those studies, he helped characterize the complex molecular machinery of the spindle assembly checkpoint, a circuit that arrests mitosis when there is spindle damage. In studies of evolution, he is best known for exploring the cellular and developmental basis for evolvability, and he co-authored two books with John Gerhart. His work in systems biology has focused on quantitative models on Wnt signaling and the fold change response in the Wnt pathway. Kirschner is a member of the National Academy of Sciences and the American Academy of Arts and Sciences, a Foreign Member of the Royal Society of London and the Academia Europaea. He has received numerous honors and awards.


Michael Levin, Ph.D. | Allen Discovery Center at Tufts University

Reading and Writing the Morphogenetic Codeundefined

Abstract: Living systems are able not just to grow tissues, but to maintain them over time and, in some cases, regenerate them when they are altered by injury or disease. Underlying this ability is the morphogenetic code, which consists of the mechanisms and information structures by which networks of cells represent and dynamically regulate the target morphology of the system.

With the ultimate goal being the top-down control of complex biological shape, we need to understand how biological systems control anatomy, from the level of tissues to the entire body plan. Control over these processes would have transformative implications for not only biology and medicine but many other disciplines.

Current technology and conceptual schemes target the level of proteins, genes and cells, but are unable to link these to large-scale anatomy. The Discovery Center team will fill this major gap by building new tools that exploit endogenous bioelectric and regulatory pathways, resulting in impactful new capabilities in regenerative medicine.

Bioelectricity is one layer of a complex morphogenic field that harnesses individual cell behavior toward the anatomical needs of the body. However, it is not simply yet another mechanism of single-cell control. Briefly altering the bioelectric connectivity of a cellular network enables permanent rewriting of an organism’s target morphology, making it a convenient and tractable entry point for understanding and rationally controlling information processing that maintains larger-scale order in vivo.

The team seeks to understand where bioelectric patterns originate, how they map the organization of cells, and how their code is interpreted by cells. This will enable the team to create the first quantitative theory of top-down pattern control, and ultimately harness new modalities for reading and writing the bioelectric code with applications in embryogenesis, regeneration, cancer and bioengineering.

Bio: Prior to college, Michael Levin worked as a software engineer and independent contractor in the field of scientific computing. He attended Tufts University, interested in artificial intelligence and unconventional computation. To explore the algorithms by which the biological world implemented complex adaptive behavior, he got dual B.S. degrees, in CS and in Biology.  He received a PhD from Harvard University for the first characterization of the molecular-genetic mechanisms that allow embryos to form consistently left-right asymmetric body structures in a universe that does not macroscopically distinguish left from right (1992-1996); this work is on Nature’s list of 100 Milestones of Developmental biology of the Century. He then did post-doctoral training at Harvard Medical School (1996-2000), where he began to uncover a new bioelectric language by which cells coordinate their activity during embryogenesis. His independent laboratory (2000-2007 at Forsyth Institute, Harvard; 2008-present at Tufts University) develops new molecular-genetic and conceptual tools to understand information processing in regeneration, embryogenesis, and cancer suppression. He holds the Vannevar Bush endowed Chair and serves as director of the Tufts Center for Regenerative and Developmental Biology. Recent honors include the Scientist of Vision award and the Distinguished Scholar Award. His group’s specific focus is on endogenous biophysical mechanisms that implement decision-making during pattern regulation, and harnessing voltage gradients that serve as prepatterns for anatomical polarity, organ identity, gene expression, and epigenetic modification. The lab’s current main directions are: 1) understanding how somatic cells form bioelectrical networks for processing pattern memories and guiding morphogenesis, 2) creating next-generation AI tools for helping scientists understand top-down control of pattern regulation (a new bioinformatics of shape), and 3) using these insights to discover new capabilities in regenerative medicine and engineering.


Scott Manalis, Ph.D. | Massachusetts Institute of Technology

"Defining Vulnerabilities of Minimal Residual Disease"undefined

Abstract: David Weinstock and Scott Manalis want to convert cancer remissions into cures. Most of the 20,000 people who die of lymphoma every year in the U.S. die of relapsed cancer — their disease was sent into remission by treatment but eventually came back, due to undetectably tiny amounts of cancer cells left behind after their therapies, also known as minimal residual disease. Luckily, technology to detect these few straggler cancer cells is improving, but researchers still don’t understand why these cells are able to escape the treatments that kill most of the other tumor cells. Weinstock and Manalis aim to tackle the difficult problem of minimal residual disease in lymphoma by developing new technologies to study these rare cells in animal models and biopsies from patient volunteers taken before treatment and after the patients go into remission. Finding the molecular differences in the cancer cells before and after remission will allow the researchers to identify why these malignant cells are uniquely dangerous, and ultimately how to better prevent the lymphomas from coming back.

Bio: Scott Manalis, Ph.D., is the Andrew and Erna Viterbi Professor of Biological Engineering and a member of the Koch Institute for Integrative Cancer Research. He has been a faculty member at Massachusetts Institute of Technology since 1999 and prior to that he received his undergraduate and graduate degrees in physics and applied physics at University of California at Santa Barbara and Stanford, respectively. His lab develops microfluidic technologies to measure biophysical properties of single cells (e.g. mass and growth rate) and uses them to characterize therapeutic sensitivity in a broad range of tumor types.


Clodagh O'Shea, Ph.D. | Salk Institute

"Assembling DNA into chromatin"undefined

Abstract: Clodagh O’Shea will tackle how the assembly of DNA into chromatin, the protein packaging system that compacts a six-foot-long string of DNA into a microscopically small nucleus, determines how drugs function, fuels cancer and drives everything about our biology. O’Shea proposes that DNA assembles highly flexible chromatin chains that adapt many different shapes and at critical concentration densities in the nucleus change states between liquids and gels. In the liquid, less concentrated state, genes are loosely bundled into dilute chromatin and can be easily accessed by proteins and read out into their protein products. In the more concentrated, gel-like phase, tightly-packed DNA keeps genes locked away and silenced. Her project will test this theory using a newly developed chromatin “paint” called ChromEMT that illuminates DNA’s 3D chromatin shape and interactions in the nucleus of intact cells and tissues. Using these new technologies, her team will ask if liquid-to-gel chromatin state transitions determine genomic DNA activity, and ultimately cell fate, in response to epigenetic drugs, aging, cancer-causing genes and viruses.

Bio: Clodagh O’Shea is the Wicklow Capital Endowed Chair and a Professor of Molecular and Cell Biology at the Salk Institute as well as a Howard Hughes Medical Institute Faculty Scholar. Her research integrates cancer biology, systems virology, structural biology, multi-modal imaging, synthetic biology and genomics to reveal critical growth regulatory targets and translate this knowledge into precision medicines. Her work has revealed the profound overlap between the cellular networks and targets disrupted in viral and cancer replication, which she is exploiting to design synthetic viral vectors, vaccines and cancer therapies. Her team has also developed disruptive new genome assembly and imaging technologies, such as Adsembly and ChromEMT. ChromEMT enables chromatin structure and 3D organization to be reconstructed  at nucleosome resolutions and megabase scales, which has revealed fundamental new insights into genome structure-function in the nucleus. Dr. O’Shea received her Bachelor’s degree in Biochemistry from the University College Cork and her Ph.D. in Immunology at the I.C.R.F. in London. She was a HFSP fellow in Dr. Frank McCormick’s laboratory at the UCSF Cancer Center where she worked on the prototype for oncolytic viral therapy. She has received numerous awards for her research, including the Beckman Young Investigator Award, the Sontag Distinguished Scientist Award, the American Cancer & Gene Therapy Young Investigator Award, Kavli Frontiers Fellow, and the W.M. Keck Medical Research Award. 


Michael Rosen, Ph.D. | The University of Texas Southwestern Medical Center

"Nuclear Organization Through Phase Separation: Mechanisms, Functions and Disease"undefined

Abstract: Many of the internal structures in our cells, or organelles, are separated by thin membranes, like small balloons within the larger balloon that is the entire cell. These separations allow different regions of the cell to carry out specialized functions, without mixing molecules with other structures in the cell. In the past several years, researchers have come to appreciate that the cell has other ways to separate its compartments that rely not on membranes, but on a process named phase separation, similar to the way oil and vinegar separate in a salad dressing. In the nucleus, the DNA-storage compartment of the cell, these phase separated compartments, also known as biomolecular condensates, appear to be especially important for how cells turn their genes on and off and how they repair their DNA when it is damaged. Michael Rosen and his team will probe the chemical properties that allow certain proteins to form condensates, study how phase separation alters gene activity, capture precise images of the condensates’ 3D structures, and ask how alterations in biomolecular condensates trigger a rare type of cancer. 

Bio: Michael Rosen is Chair of the Department of Biophysics at UT Southwestern Medical Center, where he holds the Mar Nell and F. Andrew Bell Distinguished Chair in Biochemistry and is an Investigator of the Howard Hughes Medical Institute. His lab uses biophysical techniques to understand the formation, regulation and functions of biomolecular condensates, cellular compartments that concentrate diverse but specific groups of molecules without a surrounding membrane. Applying tenets from polymer science he established multivalency-driven liquid-liquid phase separation (LLPS) as an organizing principle for biomolecular condensates. He showed that diverse multivalent molecules, including natural and engineered multidomain proteins, intrinsically disordered proteins and nucleic acids undergo liquid-liquid phase separation in vitro and in cells, forming distinct structures with unique functions. Further, he showed that assembly and disassembly of phase separated structures can be rapidly controlled by covalent modifications, elucidating a key mode of condensate regulation. Broadly, his lab illustrated how complex behaviors of condensates can be reduced to biochemically tractable problems and simple rules.


Shayn Peirce-Cottler, Ph.D. | University of Virginia & Allen Discovery Center at Stanford University

Systems Modeling of Infectionundefined

Abstract: Multiscale models that can integrate data from the levels of genes and proteins to a full cell, to collections of cells within a tissue, and ultimately to tissues and organs, is a grand challenge for systems biology. These kinds of models will be capable of predicting how perturbations at one level of scale, such as gene expression, affect important outcomes at other levels of scale, like phenotype and function.

In order to understand the molecular basis for disease—an essential to developing effective, next generation cures—we need these kinds of multiscale models that comprehensively represent whole cells, as well as their dynamic environments and interactions.

The Discovery Center team’s multiscale modeling will focus on the interaction between the pathogen Salmonella and macrophages, part of the first line of the innate immune defense. Studying and modeling this particular system will have specific, immediate impact on a global biomedical challenge of antibiotic-resistant pathogens, as well as generally enhance our understanding of complex diseases. The modeling approach the team employs will lead to the identification of better, more sophisticated antimicrobial strategies by integrating multiple biological pathways and networks, allowing for heterogeneous cellular phenotypes, including host-pathogen interactions during infection and accounting for the in vivo environment. Combined, these inputs will yield powerful, predictive and highly relevant models.

The goals of the Allen Discovery Center at Stanford  include major advances in several fields. In addition to improving whole-cell modeling of both host cells and infectious bacteria, the team will advance the modeling of interacting cells, improve computational power to boost simulation run time, create new visualization tools and employ deep learning for data analysis, and describe computational measurements of observations of cellular processes and dynamics.

Ultimately, the team’s models will suggest experiments with the highest likelihood of generating new knowledge, shortening the path to breakthroughs, and be able to predict or diagnose complex, multi-network phenotypes, both within individual cells and as a result of cell-to-cell interactions and heterogeneity.

Bio: Shayn Peirce-Cottler, Ph.D. is Professor of Biomedical Engineering with secondary appointments in the Department of Ophthalmology and Department of Plastic Surgery at the University of Virginia. She received Bachelors of Science degrees in Biomedical Engineering and Engineering Mechanics from The Johns Hopkins University in 1997. She earned her Ph.D. in the Department of Biomedical Engineering at the University of Virginia in 2002. Dr. Peirce-Cottler develops and uses computational models, in conjunction with novel experimental assays, to study complex, dynamic, and multi-cell biological systems. Her research focuses on understanding how heterogeneous cell behaviors and their interactions enable tissues to adapt over time, during physiological growth and in response to disease. Her multi-scale computational models employ agent-based modeling to bridge protein-level mechanisms with tissue-level, functional outcomes. Her research spans basic science discovery to the design of therapies for regenerative medicine. Specific areas of interest include acute and chronic inflammation, arterio-venous patterning, and the role of stem cells in orchestrating tissue regeneration. Dr. Peirce-Cottler is a past recipient of MIT Technology Review’s “TR100 Young Innovator Award” and the National Biomedical Engineering Society’s “Rita Schaffer Young Investigator Award”. She was recently elected into the American Institute for Medical and Biological Engineering College of Fellows.


Jay Shendure, M.D., Ph.D. | Allen Discovery Center at UW Medicine

Cell Lineage Tracingundefined

Abstract: Scientists have been asking questions about the ancestry and lineage of cells for over a century, but tracing the relationships between generations of cells has faced significant technical challenges. In the past several years, teams led by Jay Shendure, M.D., Ph.D., at the University of Washington, Michael Elowitz, Ph.D., and Long Cai, Ph.D., at Caltech and Alex Schier, Ph.D., at Harvard have created new technologies that take advantage of modern gene editing methods to effectively trace cells as they divide, move and differentiate throughout an organism’s development.

The Allen Discovery Center for Cell Lineage Tracing will use these new technologies and paradigms to develop lineage maps for the zebrafish and mouse – the first global maps of development in any vertebrate. They will also develop genomic systems to record the molecular events that regulate development. The Center’s other investigators are Carlos Lois, Ph.D., at Caltech and Marshall Horwitz, M.D., Ph.D., UW professor of Pathology, and Cole Trapnell, Ph.D., UW assistant professor of Genome Sciences. 

Bio: Jay Shendure is an Investigator of the Howard Hughes Medical Institute and Professor of Genome Sciences at the University of Washington. His 2005 PhD included one of the first successful demonstrations of massively parallel or next generation DNA sequencing. Dr. Shendure's research group in Seattle pioneered exome sequencing and its earliest applications to gene discovery for Mendelian disorders (e.g. Miller and Kabuki syndrome) and autism; cell-free DNA diagnostics for cancer and reproductive medicine; molecular profiling of single cells; massively parallel reporter assays and saturation genome editing; and whole organism lineage tracing. He is the recipient of the 2012 Curt Stern Award from the American Society of Human Genetics, the 2013 FEDERAprijs, a 2013 NIH Director's Pioneer Award, and the 2014 HudsonAlpha Life Sciences Prize. He serves or has served on the Advisory Committee to the NIH Director, its Working Group on the US Precision Medicine Initiative, and the National Human Genome Research Advisory Council.


Christian Steidl, M.D. | BC Cancer Research Centre and the University of British Columbia

"The microenvironment architecture and ecosystem of Hodgkin lymphoma at single cell resolution"undefined

Abstract: In cancer, healthy cells can play a huge role — not in keeping the disease in check, but in helping tumors grow. Cancer cells hijack many of our bodies’ natural processes to help themselves grow and spread and to evade detection by the immune system. Christian Steidl will study this phenomenon, also known as the tumor microenvironment, in patients with classical Hodgkin lymphoma, a blood cancer that typically strikes adolescents and young adults. This lymphoma can often be successfully treated, but as many as 30 percent of patients relapse after treatment. Steidl and his team will study patients’ lymph node samples before and after cancer relapse, cell by cell, to better understand how the genes and proteins in cancer cells and healthy cells in their ecosystem change during the course of disease. What they find could inform better ways to diagnose Hodgkin lymphoma and better, more specific treatments for the disease.  

Bio: Christian Steidl is the Research Director of the Centre for Lymphoid Cancer, Associate Vice President Research at BC Cancer and Associate Professor in the Department of Pathology and Laboratory Medicine at the University of British Columbia. He has expertise in clinical malignant hematology, molecular pathology, genomics and lymphoma biology. Dr. Steidl’s translational research group focuses on the pathogenesis of B cell lymphomas, tumor microenvironment biology and applied genomics. He is most known for his discovery and characterization of novel gene mutations in Non-Hodgkin lymphomas and microenvironment-related biomarkers in Hodgkin lymphoma. Dr. Steidl is the lead investigator of a team grant on treatment failure in lymphoid cancers funded by the Terry Fox Research Institute (TFRI), and project leader of a Genome Canada Large-Scale Applied Research Project to advance personalized treatments of lymphoid cancer patients. Dr. Steidl is a member of the Scientific Advisory Board of the Lymphoma Research Foundation, Chair of the American Society of Hematology Scientific Committee on Lymphoid Neoplasia and Member of the Leukemia and Lymphoma Society of Canada Medical and Scientific Advisory Committee. In 2017, he was inducted as a member of the Royal Society of Canada, College for New Scholars, Artists and Scientists.


Matthias Stephan, M.D., Ph.D. | Fred Hutchinson Cancer Research Center and the University of Washington

"Cutting across discipline boundaries: Bioengineering meets T-cell therapy"undefined

Abstract: Of all the forms of cancer common in the United States, lymphoma is a particularly tragic type of the disease. Considering the approximately 100,000 new cases diagnosed every year, developing more successful methods to treat lymphoma is very important. Traditionally, this condition is addressed with a combination of chemotherapy and radiation—both of which have effects that can be seriously damaging themselves. Dr. Matthias Stephan will lead the development of an alternative approach—one that programs the patient’s existing immune system to specifically attack the cancer, and thereby circumvents the damaging consequences of systemic chemical treatments. His research has established that microscopic gene-carrying nanoparticles engineered to target T lymphocytes can instruct them to destroy cancer-causing cells—a method that is not only very successful, but also avoids harmful effects caused by existing alternatives. Next, he and his team plan to scale up the production of these programming nanoparticles to clinically relevant amounts, to document their FDA credibility, and to establish the safety of their medical applications in a large animal model. Stephan expects that the end result of this project will be a product ready for clinical testing. 

Bio: Dr. Stephan began specializing in this area as a graduate student at Memorial Sloan-Kettering Cancer Center, where he pioneered auto-costimulation and trans-costimulation as molecular strategies to augment the function of lymphocytes in the microenvironment created by tumors During his postdoctoral training at the Massachusetts Institute of Technology, Dr. Stephan developed a nanoparticle-based strategy to provide autocrine sources of adjuvant growth factor that support adoptively transferred, tumor antigen-specific T lymphocytes. Much of this work became the intellectual and technical foundation for a Cambridge-based startup company (Torque Therapeutics, Inc.). The long-term goal of his ongoing research at Fred Hutch is to make immunotherapy more practical and widespread by creating unconventional treatments at the interface between materials science and immunology. For example, his group developed an innovation that allows cancer-fighting immune cells to be contained in a biopolymer and surgically implanted at tumor excision sites — which means they can begin eliminating residual cancer cells immediately. These interdisciplinary studies demonstrate for the first time that launching cancer-fighting immune cells from polymeric devices can prevent relapse, and furthermore provide a treatment option for inoperable tumors. More recently, his research group reported a strategy to program circulating T cells with tumor-recognizing activities, which avoids the complex laboratory protocols usually used to achieve this transformation. 


Jonathan Stokes, Ph.D. | Broad Institute of MIT and Harvard

"Learning to discover novel antibiotics from vast chemical spaces"undefined

Bio: Jonathan Stokes is a Banting Fellow in the Collins lab at the Broad Institute of MIT & Harvard. He received his BHSc in 2011, graduating summa cum laude, and his PhD in antimicrobial chemical biology in 2016, both from McMaster University. His current research applies a combination of chemistry, biology, and artificial intelligence to develop novel antibacterial therapies with expanded capabilities over conventional antibiotics. Dr. Stokes is the recipient of numerous awards, including the Canadian Institutes of Health Research Master’s Award, the Colin James Lyne Lock Doctoral Scholarship, and the prestigious Banting Postdoctoral Fellowship, where he ranked 1st in Canada.


Christopher Walsh, M.D., Ph.D. | Allen Discovery Center at Boston Children's Hospital

Human Brain Evolutionundefined

Abstract: The human brain is the product of remarkable evolutionary changes that have resulted in our ability to use language, create complex societies, pursue science and create art. While we have some understanding of the genes that separate all modern humans from other primates, none of those genes can explain changes in behavior that took place in the last 50,000 years, meaning there is no simple genetic “switch” that can explain key aspects of brain evolution.  

The Allen Discovery Center for Human Brain Evolution will take a multidisciplinary approach to this question, with the goals of identifying key genes required for human brain evolution, analyzing their roles in human behavior and cognition, and studying their functions to discover evolutionary mechanisms. Joining Walsh, who will be leading the center, are co-leads Michael Greenberg, Ph.D., and David E. Reich, Ph.D., at Harvard Medical School and the Howard Hughes Medical Institute, bringing together expertise in neuronal molecular biology, human evolution, genetics and genomics.

Bio: Christopher A. Walsh is Bullard Professor of Pediatrics and Neurology at Harvard Medical School, Chief of the Division of Genetics and Genomics at Boston Children's Hospital, an Investigator of the Howard Hughes Medical Institute, and an Associate Member of the Broad Institute. Dr. Walsh completed his MD and PhD degrees (with Ray Guillery) at the University of Chicago, neurology residency and chief residency at Massachusetts General Hospital, and postdoctoral training in Genetics at Harvard Medical School with Connie Cepko.  In 1993 he became Assistant Professor of Neurology at Beth Israel Deaconess Medical Center, and he has been the Bullard Professor since 1999.  He became an Investigator of the Howard Hughes Medical Institute in 2002, and from 2003-2007 served as Director of the Harvard-MIT Combined MD-PhD training program.  He moved to Boston Children’s Hospital in 2006, becoming Chief of Genetics.  Dr. Walsh’s research has focused on the development, evolution, and function of the human cerebral cortex, pioneering the analysis of human genetic diseases that disrupt the structure and function of the cerebral cortex by fostering worldwide collaborations with physicians and families.  His laboratory has identified genetic causes for more than twenty brain diseases of children, associated with autism, intellectual disability, seizures, and cerebral palsy, and has discovered that some of these disease genes were important targets of the evolutionary processes that shaped the human brain.  The work has been recognized by a Jacob Javits Award from the NINDS, the Dreifuss-Penry Award from the American Academy of Neurology, the Derek Denny-Brown and the Jacoby Awards from the American Neurological Association, the American Epilepsy Society’s Research Award, the Krieg Award from the Cajal Club, the Wilder Penfield Award from the Middle Eastern Medical Assembly, and most recently the Perl-Neuroscience Award from the University of North Carolina.  He is an elected member of the American Neurological Association, the American Association of Physicians, the National Academy of Medicine, and the American Association for the Advancement of Sciences.


David Weinstock, M.D. | Dana-Farber Cancer Institute

"Defining Vulnerabilities of Minimal Residual Disease"undefined

Abstract: David Weinstock and Scott Manalis want to convert cancer remissions into cures. Most of the 20,000 people who die of lymphoma every year in the U.S. die of relapsed cancer — their disease was sent into remission by treatment but eventually came back, due to undetectably tiny amounts of cancer cells left behind after their therapies, also known as minimal residual disease. Luckily, technology to detect these few straggler cancer cells is improving, but researchers still don’t understand why these cells are able to escape the treatments that kill most of the other tumor cells. Weinstock and Manalis aim to tackle the difficult problem of minimal residual disease in lymphoma by developing new technologies to study these rare cells in animal models and biopsies from patient volunteers taken before treatment and after the patients go into remission. Finding the molecular differences in the cancer cells before and after remission will allow the researchers to identify why these malignant cells are uniquely dangerous, and ultimately how to better prevent the lymphomas from coming back.

Bio: Dr. David Weinstock is an Associate Professor of Medicine and Pediatrics at Harvard Medical School, Associate Physician at Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Associate Member of the Broad Institute, and Affiliated Faculty at the Harvard Stem Cell Institute. His laboratory focuses on basic and translational discovery in lymphomas and leukemias using advanced technologies to interrogate and propagate primary specimens. He has developed new risk models for patients with lymphoma, defined a link between Down Syndrome and leukemia, and established an open-source repository of patient-derived xenografts. Dr. Weinstock directs a Leukemia and Lymphoma Society Specialized Center of Research that oversees basic discovery and clinical trials for lymphoma across 11 major academic centers.


Rachel Whitaker, Ph.D. | University of Illinois at Urbana-Champaign

"A Viral View of Infection Genomics"undefined

Abstract: Recent research has unearthed regions of the genome that are capable of moving rapidly between cells, creating a sea of dramatic and unpredictable genetic changes. These mobile genetic elements (MGEs) are particularly exploited by infectious bacteria, which evade antibiotics through rapid evolution driven by MGEs. While the scientific response to infectious disease has focused on identifying new ways to target and kill bacteria, antimicrobial resistance, virulence, and many other properties of pathogens are evolutionary problems driven by mobile elements. An evidence-based predictive understanding of the forces of evolution that lead to the emergence and spread of these traits is needed in order to stop them. Whitaker’s project will create models of MGEs and their evolutionary roles within a human system, and compare and refine those models against longitudinal data in order to capture and better understand this crucial evolutionary process.

Bio: Intimate and specific host-microbe symbiotic associations join microbes into the fabric of every ecosystem. The Whitaker lab focuses on the ecology and evolutionary biology of microorganisms in dynamic environments, including the human microbiome.  Whitaker uses genomic tools in simple natural environments to study microbial population dynamics and how they are shaped by interactions with mobile genetic elements.  Recent work has focused on interactions mediated by CRISPR-Cas: the exquisitely sensitive, sequence-specific immune system in Bacteria and Archaea.  The Whitaker lab has identified key signatures of the recent evolutionary history of microbes and viruses from population genomic data.  Recent work has demonstrated that virus infections can benefit their hosts through conditional mutualism and has enhanced understanding of both positive and negative impacts of viral infection.  Work in the Whitaker lab seeks to integrate molecular microbiology with evolutionary understanding of natural variation to better understand ongoing evolutionary processes in the microbial world.

Dr. Whitaker is an associate professor in the Department of Microbiology and Leader of the Infection Genomics for One Health (IGOH) Theme at the Carl R. Woese Institute for Genomic Biology at the University of Illinois at Urbana-Champaign.  Dr. Whitaker earned her Bachelor of Arts with a double major in Biology and the Science in Society Program at Wesleyan University in Middletown, CT. Whitaker received her Ph.D. in microbiology at the University of California, Berkeley with Dr. John Taylor, learning evolutionary principles, population genetics, and genomics.  A NASA graduate research fellowship enabled Whitaker to develop a new model system in the Archaea Sulfolobus, examining natural population structure and gene flow.  Whitaker’s postdoctoral research was in the laboratory of Dr. Jillian Banfield at Berkeley.  In 2018 she begins as co-director of the Microbial Diversity course at the Marine Biological Laboratories in Woods Hole.


Tony Wyss-Coray, Ph.D. | Stanford University

AHA-Allen Initiative in Brain Health and Cognitive Impairment Team Leaderundefined

Abstract: Tony Wyss-Coray, Ph.D., Professor of Neurology at Stanford University School of Medicine, has found in his studies that blood or plasma from young animals or humans can halt or slow brain aging in old mice, and may even improve symptoms for patients with mild Alzheimer’s disease. Now, he will lead a research team on a four-year project to unlock the biological secrets of youth and rejuvenation in young blood. They will search for the damaging proteins and molecules which accumulate in blood with aging, obesity and vascular disease, with the goal to neutralize these factors and protect against age-related diseases. The research team hopes to ultimately figure out how to mimic the beneficial effects of young blood to create new therapeutics for vascular dementia, Alzheimer’s disease, and other aging-related brain disorders. 

Bio: Tony Wyss-Coray is a professor of Neurology and Neurological Sciences at Stanford University, the Co-Director of the Stanford Alzheimer’s Disease Research Center, and a Senior Research Career Scientist at the Palo Alto VA. His lab studies brain aging and neurodegeneration with a focus on age-related cognitive decline and Alzheimer’s disease. The Wyss-Coray research team is following up on earlier discoveries which showed circulatory blood factors can modulate brain structure and function and factors from young organisms can rejuvenate old brains. These findings were voted 2nd place Breakthrough of the Year in 2014 by Science Magazine and presented in talks at Global TED, the World Economic Forum, Google Zeitgeist, and Tencent’s WE Summit in China. Wyss-Coray is the co-founder of Alkahest, a company developing plasma-based therapies to counter age-related diseases such as Alzheimer’s. Current studies in his lab focus on the molecular basis of the systemic communication with the brain by employing a combination of genetic, cell biology, and proteomics approaches in killifish, mice, and humans and through the development of bio-orthogonal tools for the in vivo labeling of proteins.


Carl Zimmer | The New York Times

"Braiding History: Reporting on Human Origins"undefined

Bio: Carl Zimmer is a columnist for the New York Times and the author of 13 books about science. His latest book, She Has Her Mother's Laugh: The Powers, Perversions, and Potential of Heredity, won the National Academy of Sciences Communication Award and was selected by the New York Times Book Review as a notable book of the year. He is professor adjunct at Yale University.