As one of the founding scientists at TIGR, Dr. Adams contributed extensively to the first genome sequence of a free-living organism, Haemophilus influenzae, and other microbial genomes. A co-founder of Celera Genomics, he led the DNA sequencing and genome annotation groups. He directed the Drosophila, human, and mouse genome sequencing projects, and a large-scale re-sequencing program to identify novel SNPs in humans.

From 2003-2011, Dr. Adams was Associate Professor of Genetics at Case Western Reserve University where he developed a research program in the evolution and mechanisms of antibiotic resistance in the nosocomial pathogen Acinetobacter baumannii. He also served as Director of the Genomics Core facility.

From 2011-2016, Dr. Adams was the Scientific Director and Professor at the J. Craig Venter Institute. There he directed programs that characterized genomic changes in the evolution of antibiotic resistance in hospital-acquired infections.

Dr. Adams received a B.A. in Chemistry from Warren Wilson College in Swannanoa, NC and a Ph.D. in Biological Chemistry from the University of Michigan.

Mark Adams on ORCID

My research goal is to elucidate how changes in gene expression regulation contribute to cancer. My lab focuses on characterizing the role of alternative-splicing misregulation in breast and ovarian cancer by using 3D cell culture and PDX models. Our unique expertise in both RNA biology and cancer research allows us to connect these distinct fields, and by combining innovative tools and interdisciplinary approaches, to gain novel insights into the molecular mechanism of gene expression regulation in normal and cancer cells. My research findings should lead to the development of novel biomarkers and promising drugs for cancer therapy.

See a recent article "Splicing factor to blame in triple negative breast cancer" on UCONN Today.

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Olga Anczukow on ORCID

I am broadly interested in two main aspects of genetics, heredity and variation. My lab focuses on how natural genetic variation shapes genome function in development. My lab combines both experimental bench work and computational methods to explore the impact of genetic variation on chromatin state and gene regulation. I have established expertise in a variety of quantitative approaches including functional genomics, proteomics, bioinformatics, and systems genetics. During my time at The Jackson Laboratory I have applied my broad skills in molecular biology to develop new functional genomic tools to investigate the role of epigenetic modifications on meiotic recombination and chromosome organization. Together this work demonstrated that meiotic chromatin undergoes a dynamic epigenetic reprogramming important to facilitate proper gamete formation. My lab now is focused on determining how genetic variation influences the epigenome and how these molecular features shape bias in early differentiation using embryonic stem cells as model systems.

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The mechanisms governing non-recurrent human structural variation (SV) are diverse and often poorly understood. I am investigating how human DNA maintains fidelity in the context of a repetitive genome. For example, human Alu elements number over one million copies per human genome, and recent studies have found that these repeat sequences often mediate SVs in some loci. Through computational, molecular biological and genomic techniques, we will identify regions susceptible to this form of SV and investigate the enzymes that limit or promote Alu-mediated rearrangements. These lines of inquiry could find regions prone to instability in human cancers and lead to targets for therapy.

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Christine Beck on ORCID

My research focuses on functional and comparative genome informatics. I work on the development of systems to integrate and analyze genetic, genomic and phenotypic information. I am one of the principal investigators of the Gene Ontology (GO) Consortium, an international effort to provide controlled structured vocabularies for molecular biology that serve as terminologies, classifications and ontologies to further data integration, analysis and reasoning. My interest in bio-ontologies stems as well from the work I do as a principal investigator with the Mouse Genome Informatics (MGI) project at The Jackson Laboratory. The MGI system is a model-organism community database resource that provides integrated information about the genetics, genomics and phenotypes of the laboratory mouse. My current research projects combine bio-ontologies and database knowledge systems to analyze disease processes with the objective of discovering new molecular elements and pathways that contribute to particular pathologies such as respiratory diseases. 

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Judith Blake on Orcid

Over a century after Cajal’s Nobel Prize for the Neuron Doctrine, we are finally beginning to combine the power of genetic engineering with high resolution microscopy to untangle the brain’s neural circuitry. Using a combination of transgenic mice, viral tools, large-volume yet high-resolution imaging, and computational techniques, my work has shown that neurons are wired in precise ways that drive specific forms of cellular and circuit computations.

My present work is focused on how such wiring supports the flexible use of behaviors, and how these wiring patterns relate to susceptibility or resilience in genetic models of neurodegenerative diseases. We will test our hypotheses using a variety of experimental approaches including array tomography, electron microscopy, rabies circuit tracing, calcium imaging, and chemogenetic perturbations in awake, behaving mice. Ultimately, a detailed understanding of the relationship between neural circuit structure and cognitive function will be necessary to fully comprehend how brain function and dysfunction emerge from its constituent cell types.

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Erik Bloss on Figshare

    Erik Bloss on ORCID   

Germ cells are the only cell type that must endure extensive DNA damage in the form of programmed meiotic double-strand breaks (DSBs) during their normal development. Paradoxically, the absence of DSBs during meiosis as well as persisting unrepaired breaks are detrimental and typically result in meiotic arrest and infertility. Our research aims to understand the molecular mechanisms controlling the development of healthy gametes and how misregulation of these mechanisms can lead to reproductive disorders. In particular, we are interested in meiotic “quality checkpoints” operating in germ cells, which ensure that the correct and intact genetic information is transmitted to the next generation. The same checkpoint that monitors DSB repair during meiosis is responsible for high sensitivity of oocytes to cancer treatment. Chemo and radiation therapies can cause oocyte death and lead to premature ovarian failure and infertility. Disabling the key checkpoint kinase CHK2 preserved fertility in mice exposed to ionizing radiation, thus opening a new avenue for oncofertility research. Our goal is to further dissect the DNA damage response pathway in oocytes, helping identify additional targets for fertility preservation therapies in cancer patients.

Geneticists measure time in generations and celebrate immortality with reproductive success. My lab is driven by a passion to understand the cell biological basis of gamete (sperm and egg) development. We study how germline stem cells balance self-renewal with differentiation. Stem cell self-renewal at the expense of differentiation can cause germ cell tumors while differentiation at the expense of self-renewal can cause sterility. Our long-term goal is to understand the mechanisms that regulate germline stem cell fate. Other research interests include understanding the molecular function of the hormone testosterone in spermatogenesis. Our work has revealed that specialized tight junctions between Sertoli cells, which are integral to the blood/testis barrier, are regulated by testosterone. We are studying how germ cells pass through these tight junctions without compromising barrier function. We are also investigating molecular mechanisms of translational regulation—a major form of gene regulation in both male and female germ cells—during spermatogenesis. We use both forward and reverse genetics to identify the genes involved. Phenotypic analysis includes microscopy, biochemistry and cell physiology.

The primary theme of my personal research program is “bridging the digital biology divide,” reflecting the critical role that informatics and computational biology play in modern biomedical research. I am a Principal Investigator in the Mouse Genome Informatics (MGI) consortium that develops knowledgebases to advance the laboratory mouse as a model system for research into the genetic and genomic basis of human biology and disease (http://www.informatics.jax.org). Recent research initiatives in my research group include computational prediction of gene function in the mouse and the use of the mouse to understand genetic pathways in normal lung development and disease.

My institutional responsibilities at The Jackson Laboratory include serving as the Deputy Director of the Cancer Center and as the Scientific Director of our Patient Derived Xenograft (PDX) and Cancer Avatar program. The PDX program is a resource of deeply characterized and well-annotated "human in mouse" cancer models with a focus on bladder, lung, colon, breast and pediatric cancer. This resource is a powerful platform for research into basic cancer biology (such as tumor heterogeneity and evolution) as well as for translational research into mechanisms of therapy resistance and therapeutic strategies to overcome resistance.

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The Burgess lab seeks to understand the molecular mechanisms of synapse formation and maintenance at two sites in the nervous system: the peripheral neuromuscular junction and the retina. In all of these studies, we are addressing basic molecular mechanisms, but these basic mechanisms have relevance to human neuromuscular and neurodevelopmental disorders. Our continued research on the genetics underlying these disorders, and our continuing effort to identify new genes involved in these processes, will increase our understanding of the molecules required to form and maintain synaptic connectivity in the nervous system.

Contemporary technologies such as high-throughput genome sequencing now enable the measurement of biological systems with unprecedented scale, power and precision, creating the opportunity to decipher the genetics that underlie human diseases. The overall goal of our laboratory is to develop novel computational strategies that use these data to understand complex genetic systems in which multiple genes and environmental factors combine to affect biological outcomes. These methods aim to map complex genetic architecture and infer models that predict the outcomes of genetic and environmental variation. We derive network models of interacting genes, integrate disparate phenotypic and molecular data types, critically evaluate models with experimental tests, and seek to understand how biological information is encoded in genetic networks and genomic data.

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Metabolism is a set of biochemical transformations, which remains the single most fundamental force driving cell fate and sustaining life. Our lab is particularly interested in understanding the cellular and molecular mechanisms that control immune cell behavior during disease development. Our investigation is currently focused on elucidating the metabolic events involved in T cell reprogramming in tumor microenvironment. Our research lies at the intersection of immunology, metabolism, microbiology, oncology, pharmacology, and bioinformatics. Ultimately, our goal is to provide detailed mechanistic understanding of metabolic interplay between immune cells and diseased tissues, which will offer novel strategies for vaccines, drug development, disease prognosis, and immunotherapy.

My laboratory integrates quantitative genetics, bioinformatics and behavioral science to understand and identify the biological basis for the relationships among behavioral traits. We develop and apply cross-species genomic data integration, advanced computing methods, and novel high-precision, high-diversity mouse populations to find genes associated with a constellation of behavioral disorders and other complex traits. This integrative strategy enables us to relate mouse behavior to specific aspects of human disorders, to test the validity of behavioral classification schemes, and to find genes and genetic variants that influence behavior.

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Broad advances in sequencing, imaging, and machine learning are rapidly transforming the nature of biology research, providing rich avenues for discovery at the nexus of experimentation, mechanistic modeling and neural network analysis. My lab uses computational, mathematical, and high-throughput data generation approaches to study how cancer ecosystems function, evolve, and respond to therapeutic treatment. We study problems in cancer sequence and image analysis across a wide spectrum of cancer types, with particular expertise in breast cancer and patient-derived xenografts.

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         Jeffery Chuang on ORCID          

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Our lab is actively applying a systems approach to study the genetics of health and disease, incorporating new statistical methods for the investigation of complex disease-related traits in the mouse. We employ a combination of strategies to investigate the genetic basis of these complex traits. We are developing new methods and software that will improve the power of quantitative trait loci mapping and microarray analysis, as well as graphical models that aim to intuitively and precisely characterize the genetic architecture of disease.

Within the Center for Genome Dynamics, we are part of a consortium of investigators with a shared interest in a holistic approach to understanding genetics from an evolutionary perspective. With an eye on the future of mouse genetics, we are also establishing two new mouse resources for complex trait analysis: the Collaborative  Cross and the Diversity Outbred.

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Our lab uses mouse models to identify the molecular pathways underlying degenerative motor neuron diseases in humans, such as spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease). We cloned the gene for neuromuscular degeneration in a mouse model for a lethal infantile form of SMA known as spinal muscular atrophy with respiratory distress. In addition, we are studying genetic background effects on onset and progression of ALS symptoms in the mouse model in hopes that these will provide novel targets for therapy.

We are also studying mice with degenerative muscle diseases that are models for specific forms of muscular dystrophy in humans. We cloned a genetic defect and have localized the mutation to the muscle-specific titin gene, the largest known coding gene in the mammalian genome. The mouse strain is a novel model of progressive muscular dystrophy. We also identified the mutation for a new form of rostrocaudal muscular dystrophy that affects skeletal muscle tissues with an unusual front-to-back severity of symptoms. We now have an excellent model for this childhood disorder to learn about the molecular causes of disease and to test for potential therapeutic strategies.

Mutation, recombination, and chromosome assortment account for all genetic diversity in nature, ranging from variants associated with disease to adaptive genetic changes. Despite their fundamental significance to genetic inheritance, the frequencies of mutation and recombination and the strength of chromosome transmission biases vary tremendously among individuals.

The broad objective of my research group is to understand the causes of variation in the very mechanisms that generate genetic diversity. Toward this goal, we pursue two complementary research strategies. First, we leverage the recognition that mutation rate, recombination frequency, and biased chromosome transmission are themselves complex genetic traits controlled by multiple genes and their interactions. We combine cytogenetic and genomic approaches for assaying DNA transmission with quantitative genetic analyses in order to identify the genetic and molecular causes of variation in these mechanisms. Second, through targeted investigations of loci with extreme recombination or mutation rates, we aim to illuminate the biological mechanisms that stimulate or suppress these processes. We are currently using this latter approach to investigate recombination rate regulation, patterns of genetic diversity, and the evolutionary history of the mammalian pseudoautosomal region.

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Our lab uses multi-omics systems biology approaches to study blood pressure regulation, cardiovascular genomics and epigenomics, as well as membrane and cellular proteins and their role in cell signaling and cell-cell interaction. Our work has helped to characterize the renin-angiotensin system at the cellular, molecular, and whole animal levels and has helped to define the role of the renin-angiotensin-aldosterone system in angiogenesis. We created and characterized the first renin knockout rat, and explored the molecular regulation of renin in salt-sensitive hypertension. We were also among the first to recognize the importance of bone marrow derived mononuclear and endothelial progenitor cells in angiogenesis and have published several key papers describing the importance of gene-environment interaction in the competency of these cells. Our laboratory is also interested in developing techniques for the study of genes and proteins and their interactions in physiological systems.

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The Handel laboratory investigates the genetic regulation of meiosis and spermatogenesis and male fertility. Meiosis is the specialized cell division, unique to germ cells, that reduces the number of chromosome sets from two (diploid) to one(haploid), thus producing the egg and sperm gametes that come together during sexual reproduction. Appropriate dynamics and behavior of chromosomes during meiosis are essential to genetic integrity and reproductive success. Our investigations focus on factors extrinsic and intrinsic to meiotic chromosomes that establish meiotic chromosome structural transitions in both male and female germ cells and identify sexually dimorphic events. From our endeavors, significant new information is emerging about how germ cells program meiotic events, and ultimately this will help us understand how errors in meiotic mechanisms lead to aneuploidy, or inappropriate chromosome number, producing developmental abnormalities in offspring.

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The Harrison research group investigates aging in mouse models, focusing on processes that have the potential to retard aging and prolong health. For example, one line of research investigates mutations that reduce IGF-1 and insulin function. Such mutations can increase life span and delay certain aspects of aging, especially development of cancer. We also demonstrated through an Intervention Testing Program (ITP) that rapamycin, an inhibitor of the mTOR pathway, extends median and maximal lifespan in mice. We are continuing our ITP research.

Our other focus area is on hematopoietic stem cells (HSCs) and other adult stem cells, which constantly proliferate and differentiate to maintain tissue functions throughout life. If aging exhausts the function of adult stem cells, the balance between damage and repair is disrupted and tissue functions become defective. Our group has found that genetic mechanisms protect hematopoietic stem cells from exhaustion in some mouse strains, and we are working to define the specific mechanisms. Our long-term goal is to promote healthful aging in humans, either by delaying normal aging processes or by minimizing or eliminating diseases of aging.

J. Travis Hinson, M.D., utilizes genomic approaches like CRISPR/CAS to interrogate mechanisms of inherited cardiovascular disorders especially those that lead to heart failure. He is particularly interested in developing single cell and cardiac microtissue assays derived from disease-specific, human induced pluripotent stem cells (iPScs) in combination with in vivo mouse models. His lab’s current research focus is:

1. To define the role of AMP-activated protein kinase in physiologic and pathologic forms of cardiac remodeling.
2. To engineer cardiac microtissues to study the most common forms of familial hypertrophic and dilated cardiomyopathies due to sarcomere mutations. 
3. To develop assays for high-throughput functional genomic screens to predict pathogenicity of genetic variation in cardiomyopathy genes. 

These studies capitalize on the Laboratory’s expertise in human genetics, stem cell biology, tissue engineering and computational methods. While my laboratory is at the Jackson Lababoratory, I also maintain a clinical practice treating patients with inherited cardiovascular diseases at the University of Connecticut Cardiology division. 

In the Howell lab, we apply genetics and genomics approaches to identify fundamental processes involved in the initiation and early propagation of age-related neurodegenerative diseases, focusing on Alzheimer's disease, non-Alzheimer's dementia and glaucoma. Understanding these processes provides the greatest opportunity of therapeutic intervention. We are particularly interested in the role of non-neuronal cells including astrocytes, monocyte-derived cells (such as microglia), endothelial cells and pericytes.

In previous work, I applied novel genomics and bioinformatics strategies to identify new molecular stages of glaucoma that preceded morphological changes. Genetic knockout and/or pharmaceutical approaches showed that targeting the complement cascade and endothelin system significantly lessened glaucomatous neurodegeneration in mice. Our work with glaucoma continues in collaboration with Dr. Simon John, and we are also now applying similar genetics and genomics strategies to understand initiating and early stages of Alzheimer's disease, vascular dementia and other dementias. A major aim is to combine knowledge from human genetic studies with the strengths of mouse genetics to develop new and improved mouse models for dementias and make them readily available to scientific community.

Gareth Howell at University of Maine

    Gareth Howell at Tufts University 

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I received my PhD in Neuroscience from University College London (UCL) where I trained with Dr. Patrick Anderson. My work focused on understanding molecular mechanisms that can be targeted for axonal regeneration in the injured spinal cord. Towards the end of my PhD, I became interested in projections upstream of the spinal cord, in the brain, where connections are more plastic. To further my understanding in reparative mechanisms in the brain, I undertook postdoctoral training with Dr. S.Thomas Carmichael at UCLA, where I studied molecular mechanisms that underlie plasticity during learning and memory as targets for stroke. In addition to molecular targets, I became interested in how neural circuits interact during movement, a domain that is compromised in stroke patients. For further training, I was awarded a visiting fellowship at Janelia, HHMI, where I worked with Dr. Adam Hantman, where I used a unique imaging platform to visualize and target circuit activity across multiple regions in the brain to determine how motor information is encoded in real-time in the normal brain. In my current lab, using a combination of techniques, we will determine how circuits re-organize after a stroke, how these re-organizational processes contribute to changes in motor function, molecular mechanisms that enhance plasticity in these circuits and therapeutic targets that can be clinically translated.

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Mary Teena Joy on ORCID

To get a different answer you need to ask the question differently.

Alzheimer’s disease currently affects 5 million Americans and despite decades of research we do not yet have a treatment that can even substantially slow the devastating symptoms let alone cure the inevitable cognitive decline.  Work in my laboratory to address this situation was launched not by asking what causes the disease, but by posing the counterintuitive question: “What makes some people resistant to the disease”?  In looking for the answer to this disarmingly simple question my laboratory is now leading a unique attack on Alzheimer’s and age-related dementia by focusing on identifying and validating the genetic factors that protect individuals from cognitive decline.

Integrated with broad collaborative efforts, my team of interns, research scientists, postdoctoral fellows and graduate students are working on a variety of projects that seek to understand these “genetic mechanisms and biomarkers of resilience” with the ultimate goal of turning these protective factors into novel therapies.

Chronic kidney disease (CKD) is a growing medical problem, and the number of patients progressing to end-stage renal disease has increased by 95 percent over the last 10 years in the United States. There are currently over half a million Americans on dialysis, a procedure that severely reduces quality of life and comes with much comorbidity. Furthermore, the impact of CKD is not limited to impairments related to renal failure. CKD is also recognized as an important risk factor for other ailments such as cardiovascular disease, including myocardial infarction, atherosclerosis, stroke and hypertension. A critical and unavoidable contributor to CKD is normal kidney aging.

Our goal is to identify key genetic factors that contribute to the decline of function and damage in the aging kidney, to learn their role in the kidney, and to understand why variations of these factors lead to different outcomes. We do this by studying the natural genetic variation in mice and their association with different kidney phenotypes. Once causal genes are identified, we develop precision disease models for further study of the gene and to develop therapeutics that will slow down the decline of kidney function and development of disease.

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The Kumar Lab consists of geneticists, neuroscientists, and computer scientists. We are passionate about discovering novel targets and models for mental illness through innovation at the confluence of computational, genetic, and genomic methods. Broadly, we are interested in development of better animal models and animal phenotyping methods for human psychiatric illnesses. We use computer vision approaches to quantitate behavior and functional approaches to understand its underlying neuronal and genetic architecture. We have developed high-throughput computer vision based methods for ethologically relevant animal phenotyping. In functional genomics work, we use QTL and mutagenesis approaches to discover novel pathways that can be targeted for addiction therapeutics. Our approaches are flexible and can be applied towards many psychiatric phenotypes. In sum, we are a leading research group using genetics as its foundation, and a combination of biochemistry, physiology, imaging, and computer vision techniques to dissect complex behavior in mammals.

Dr. Kumar carried out undergraduate research at The University of Chicago with Dr. Bob Haselkorn. He received his PhD at UCSD working with Dr. Michael G. Rosenfeld and structurally and biochemically characterized transcriptional co-repressors. During his postdoctoral work, Dr. Kumar trained with Dr. Joseph S. Takahashi at Northwestern and UT Southwestern and worked on functional genomics approaches to dissect the genetics of addiction.

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Ching Lau serves as the Medical Director of Hematology-Oncology at Connecticut Children’s, as Professor at JAX where he specializes in pediatric brain and bone tumor research, and as Head of the Division of Pediatric Hematology-Oncology in the Department of Pediatrics at the UConn School of Medicine. His clinical interests include neuro-oncology, solid tumors, and osteosarcoma.

The research laboratory of Dr. Charles Lee at The Jackson Laboratory for Genomic Medicine develops and applies state-of-the-art technologies to study structural genomic variation and its contribution to human diseases, and vertebrate genome evolution.

Dr. Lee’s primary interest is to understand the role of signaling molecules in regulating embryonic development and adult tissue homeostasis. He has focused on the superfamily of secreted proteins that are structurally related to transforming growth factor-Β (TGF-Β). Members of this growth factor family have been shown to play important roles in regulating the development and function of many different tissues, and as a result, many of these factors have shown enormous therapeutic potential for a wide range of clinical applications. Using molecular genetic approaches, he and his lab have identified a large number of novel mammalian TGF-Β family members that we have designated growth/differentiation factors (GDFs). They have been using a variety of experimental approaches, including genetic manipulation of mice, to attempt to understand the precise biological functions of these molecules. We are particularly interested in understanding the roles of these molecules in regulating tissue growth.

Much of his work has focused on a molecule that he and his team have designated myostatin. They have shown that myostatin is expressed specifically in developing and adult skeletal muscle and that mice engineered to lack myostatin exhibit dramatic increases in skeletal muscle mass throughout the body. Based on these and other studies, they believe that myostatin normally acts to block skeletal muscle growth.

Dr. Lee and his team are currently attempting to elucidate the mechanism of action of myostatin as well as the mechanisms by which the activity of myostatin is regulated. Their long term goal is to attempt to exploit the biological properties of myostatin to develop novel therapeutic strategies for treating patients with muscle degenerative and wasting conditions, such as muscular dystrophy, sarcopenia, and cachexia resulting from diseases like cancer, AIDS and sepsis.

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The application of high-resolution mass spectrometry now enables the measurement in human samples the metabolome, lipidome and small molecules of dietary, microbial and environmental origins. This revolutionary information fills a major gap between genome and environment, with broad applications to diseases and precision medicine. We combine experimental approaches with computational algorithms that identify pathway patterns and integrate chemical reactions and biology. 

Current projects:

1. Probabilistic metabolite and network models for metabolomics. This includes the Mummichog Project, and addresses challenges in the assembly of information in metabolomics.
2. Reconstruction of biochemical networks and application to immunometabolism. The goal is to upgrade genome scale metabolic models by mass spectrometry data, via a combination of computational, genetic, cellular and isotope tracing techniques.
3. Multi-omics, multiscale modeling of human immunology. We are generating lakes of data from vaccine studies. Coupled with large-scale data mining and new generation of artificial intelligence, the resulting models shall aid vaccine development, immunotherapy and the fight against many diseases.

Shuzhao Li on Google Scholar

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My research interest is to understand the inner workings of cancer cells – the genetic and epigenetic heterogeneity that drive cancer initiation and progression. We utilize computational and sequencing methodologies to identify and characterize the essential epigenetic lesions that guide cancer cells to evolve and escape from anti-cancer therapy. The ultimate goal is to develop novel methods to predict and address tumor evolution.

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Sheng Li Personal Lab Site

Jackson Laboratory Professor, President Emeritus, and Honorary Fellow Edison Liu, M.D., focuses on the functional genomics of human cancers, particularly breast cancer, uncovering new oncogenes, and deciphering on a genomic scale the dynamics of gene regulation that modulate cancer biology.

From 2011 to 2021, Dr. Liu was the president and CEO of The Jackson Laboratory, an independent research institute focused on complex genetics and functional genomics. During his tenure, JAX grew significantly in revenue, employee headcount, international presence, research scope, philanthropy and physical footprint. Under Liu’s leadership, JAX established The Jackson Laboratory for Genomic Medicine in Farmington, Conn., and added production facilities in Ellsworth, Maine and Japan and established a joint venture in China to the institution’s headquarters campus in Bar Harbor, Maine, and production facility in Sacramento, Calif.

Previously, he was the founding executive director of the Genome Institute of Singapore and the president of the Human Genome Organization (HUGO). He was also the scientific director of the National Cancer Institute's Division of Clinical Sciences in Bethesda, Md., where he was in charge of the intramural clinical translational science programs. In his earlier career, Dr. Liu was a faculty member at the University of North Carolina at Chapel Hill, where he was the director of the UNC Lineberger Comprehensive Cancer Center's Specialized Program of Research Excellence in Breast Cancer; the director of the Laboratory of Molecular Epidemiology at UNC's School of Public Health; and the Chief of Medical Genetics.

Dr. Liu is an international expert in cancer biology, systems genomics, human genetics, molecular epidemiology and translational medicine. He has authored more than 320 scientific papers and reviews and co-authored two books. He obtained his B.S. in chemistry and psychology, as well as his M.D., at Stanford University. He then received his residency and fellowship training at Washington University, St, Louis, and Stanford, and postdoctoral training in molecular oncology at the University of California at San Francisco.

Throughout his career Dr. Liu has received numerous accolades and awards, including the AACR Rosenthal Award and the Brinker International Award, both for breast cancer research; the Public Service Medal from the President of Singapore for his contributions to resolving the SARS crisis; and the Chen Award for Distinguished Academic Achievement in Human Genetics. He was elected to the American Society of Clinical Investigation, as President of the Human Genome Organization (HUGO), as a foreign member of the European Molecular Biology Organization, and as a Fellow of the American Association for the Advancement of Science (AAAS). He holds honorary degrees from Queen’s University (Belfast, Northern Ireland), University of Southern Maine, and Colby College (Waterville, Maine).

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It has become clear that genetic background, including both common and rare variants, significantly influences disease susceptibility, severity, prognosis and even treatment effectiveness. Most genetic variants assert subtle effects in isolation, but certain combinations can disrupt normal homeostasis and sensitize an individual to disorder. Thus, many complex diseases have resisted classification by single-gene experimental and/or statistical modeling approaches. A comprehensive characterization of the genetic etiology of complex disorders and disease must account for the effects of all inputs (e.g. genetic variation) on all outputs (e.g. transcription, measures of structure/function) in the context of the affected system. 

My overarching research goals are to 1) characterize the transcriptional network architecture underlying normal organ development and homeostasis, 2) predict the genes, gene-gene interactions, and coregulated gene cohorts with major roles in this process, and 3) identify and validate genetic mutations with individual small effects that together disrupt the buffering capacity of the transcriptional network and cause a disordered/disease state. To that end, I take a systems genetics approach that integrates advanced computational methods and experimental validation techniques to next-generation genetic mapping populations, including the mouse Collaborative Cross and Diversity Outcross, to elucidate and compare the transcriptional network structure and dynamics driving organogenesis (the embryonic gonad at the critical time point of primary sex determination) and adult tissue homeostasis (liver).

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The cochlea is an incredibly complex, but well-designed organ. Precise patterning across its width is linked to neural connections going to or from the brain. These different neurons serve, respectively, to convey sound to the brain, or to dampen the signal in the presence of very loud sounds. We are interested in how patterning is determined under the context of multiple signaling pathways.

Research in my laboratory focuses on two major areas: dissecting the genetic mechanisms of mammalian development, with a focus on craniofacial development and dysmorphology, and developing new genetic tools and resources for the scientific community. We have a longstanding interest in the genes and mechanisms that govern neural crest formation, migration and differentiation. Defects in these processes often result in craniofacial abnormalities. We take both forward and reverse genetic approaches to identify new genes and pathways involved in neural crest and craniofacial development, taking advantage of unique tools and resources available at JAX. We are also working with a number of clinical collaborators, using CRISPR/Cas9 to model novel mutations hypothesize to cause a variety developmental disorders including congenital heart disease and craniofacial malformations.

Supporting this basic research interest, a significant portion of the lab effort is dedicated to developing new mouse genetic resources for the scientific community. This includes development of Cre driver resources and the JAX Knockout Mouse Phenotyping Program (KOMP2). The overarching goal KOMP2 and its partners in the International Mouse Phenotyping Consortium (IMPC) is to generate and phenotype a genome-wide set of knockout mice to build a comprehensive catalogue of gene function. As part of this effort, we have established a high-throughput platform to identify and characterize novel essential mouse genes (embryonic lethal) using advanced imaging techniques such as embryo microCT and optical projection tomography (OPT). This platform not only provides numerous new gene targets for further examination, it also serves as a key tool for our efforts to rapidly model human developmental disorders in mice. Our Cre driver program involves both generation of novel cre driver lines for the scientific community and a pipeline for characterization of both new and existing lines.

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Obesity and Type 2 diabetes mellitus (T2D) are highly prevalent metabolic diseases that afflict a large proportion of the aging population in the United States. Nearly 40 percent of adults are obese, and about 10 percent of individuals over 65 have T2D. These diseases, together with cardiovascular disease, should be viewed as aspects of a metabolic syndrome that is a result of the interaction of many genes, rather than a collection of separate entities. To illustrate the complexity of the issue, there are approximately 500 to 1,000 genes in mice that may lead to obesity when mutated. Our program aims to identify new obesity and type 2 diabetes mutations and their genetic modifiers and to determine how the underlying mutations cause the disease phenotype.

One focus of our investigations are ciliopathies (diseases caused by impaired function of primary cilia), which combine aspects of metabolic syndrome with sensory loss. Our laboratory identified a human gene, ALMS1, that is mutated in patients with Alström syndrome, a rare inherited condition characterized by childhood obesity, retinal and cochlear (inner ear) degeneration, type 2 diabetes, proliferative and dilated cardiomyopathy, hepatosteatitis, and kidney disease.

Approximately 50 million people worldwide are blind and ~150 million are significantly vision-impaired. Except for trauma and infections, the majority of human eye diseases are genetic in nature. Initially, the goal of our research program was to use mouse models as an entry point to identify the molecules that were essential for normal retinal development and function through positional cloning efforts. We have identified the molecular basis of >100 models, discovered through spontaneous and chemically induced screening.

With the maturation of our program, we have begun to focus on using these models to study gene function and mechanisms underlying disease pathology. Knowledge of genetic modifiers and interaction partners is critically important in understanding the pathways that lead from a primary genetic defect to an observable phenotype. The overriding theme of our program currently is the elucidation of interactions that occur among molecules to identify common functional pathways as well as pathways that lead to disease and are impacted by primary mutations. We employ a blend of marker analyses, noninvasive imaging, functional studies, and generation of mouse resources that aim toward a greater understanding of the function and pathways in which the mutant retinal molecules we have identified act.

Kristen O’Connell’s research program is focused on understanding the impact of diet, body weight and peripheral hormone signaling on neuronal excitability and plasticity in the hypothalamus and other brain regions associated with the regulation of food intake and body weight.

Our central goal is to develop microbiome therapeutics to treat human disease. We use diverse tools like genomics and synthetic biology to investigate our microbiome’s role in our health and engineer therapeutics.

My laboratory specializes in human immunology with a focus on experimental immunotherapy. We have pioneered the development of dendritic cell-based vaccines for patients with cancer or HIV, and I am very interested in understanding how vaccines work and precisely defining the immune mechanisms that underpin successful vaccination. We apply cutting-edge genomic approaches that offer unprecedented insights into the inner workings of immune cells (single-cell genomics, hybrid sequencing and long RNA reads).This knowledge can catalyze the discovery and development of novel immunotherapies,including vaccines that target cancer.

Karolina Palucka on ORCID

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Wu TC, Xu K, Martinek J, Young RR, Banchereau R, George J, Turner J, Kim KI, Zurawski S, Wang X, Blankenship D, Brookes HM, Marches F, Obermoser G, Lavecchio E, Levin MK, Bae S, Chung CH, Smith JL, Cepika AM, Oxley KL, Snipes GJ, Banchereau J, Pascual V, O’Shaughnessy J, Palucka K. IL-1 receptor antagonist controls transcriptional signature of inflammation in patients with metastatic breast cancer. Cancer Res. 2018 Sept 15; 78(18): 5243-5258. doi: 10.1158/0008-5472.CAN-18-0413. PubMed PMID: 30012670.

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Martin Pera was amongst a small group of researchers who pioneered the isolation and characterization of pluripotent stem cells from human germ cell tumours, studies that provided an important framework for the development of human embryonic stem cells. His laboratory at Monash University was the second in the world to isolate embryonic stem cells from the human blastocyst, and the first to describe their differentiation into somatic cells (precursors of the central nervous system). Currently his lab studies the regulation of self-renewal and pluripotency, heterogeneity in pluripotent stem cell populations, and neural specification of pluripotent stem cells. His work on neural differentiation of human pluripotent stem cells led to the development of a new treatment for macular degeneration, a common form of blindness, which is now in clinical trial in Israel. He has provided extensive advice to state, national and international regulatory authorities on the scientific background to stem cell research, and has delivered hundreds of commentaries for print and electronic media on stem cell research, ethics, and regulatory policy. At the Jackson Laboratory Pera will continue work on the regulation of pluripotency, and will study the genetic basis of individual differences in the response of the central nervous system to injury.

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Dr. Reinholdt’s research interests are in the development and application of genetic approaches for understanding the etiology and functional consequences of genome variation in the germ line and in pluripotent cells. Dr. Reinholdt is also committed to genetic resource development and has made significant contributions to the early development of high throughput sequencing approaches for genomic discovery in the mouse genome, and more recently the development of novel ES and iPSC cell lines from genetically diverse mice that are enabling platforms for cellular systems genetics.

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My group mainly focuses on elucidating how mesenchymal lineage cells (mesenchymal stem cells and fibroblasts) and immune-regulatory myeloid cells (neutrophils and macrophages) modulate the adaptive immune responses in cancer treatment resistance and metastatic relapse. These studies will fully take advantage of the unique research platform--patient-derived xenograft (PDX) tumors in humanized mouse models at The Jackson Laboratory, with the research goal to develop novel strategies targeting tumor microenvironment to improve the efficacies of conventional cancer therapies and new therapeutics such as immunotherapy.

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           Gary Ren on ORCID         

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Our main focus is the Gene Expression Database (GXD), which captures and integrates mouse expression data generated by biomedical researchers worldwide, with particular emphasis on mouse development. Gene expression data can provide researchers with critical insights into the function of genes and the molecular mechanisms of development, differentiation and disease. By combining different types of expression data and adding new data on a daily basis, GXD provides increasingly complete information about expression profiles of transcripts and proteins in wild-type and mutant mice. We work closely with the other Mouse Genome Informatics (MGI) projects to provide the community with integrated access to genotypic, expression and phenotypic, and disease-related data. Thus, one can search for expression data and images in many different ways, using numerous biologically and biomedically relevant parameters.

Peter Robinson studied Mathematics and Computer Science at Columbia University and Medicine at the University of Pennsylvania. He completed training as a Pediatrician at the Charité University Hospital in Berlin, Germany.  His group developed the Human Phenotype Ontology (HPO), which is now an international standard for computation over human disease that is used by the Sanger Institute, several NIH-funded groups including the Undiagnosed Diseases Program, Genome Canada, the rare diseases section of the UK's 100,000 Genomes Project, and many others. The group develops algorithms and software for the analysis of exome and genome sequences and has used whole-exome sequencing and other methods to identify a number of novel disease genes, including CA8, PIGV, PIGO, PGAP3, IL-21R, PIGT, and PGAP2. 

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Dr. Robson is a molecular cell biologist utilizing advanced technologies to understand the cellular composition of tissues, their development, and progression to disease. After graduate school (University of Toronto/Hospital for Sick Children) and postdoctoral studies (Children’s Hospital of Philadelphia) he started his independent laboratory at the Genome Institute of Singapore in the heart of Southeast Asia living less than a mile from the primary rain forest where Sir Alfred Russel Wallace began his field studies leading to his seminal work described in The Malay Archipelago. In Singapore, Dr. Robson made significant contributions to our understanding of the transcriptional regulatory programs controlling pluripotent stem cells and preimplantation development. An advocate of the Cell Theory defining the cell as the basic structural unit of all living systems, his lab was one of the first to exploit single cell technologies to identify molecular mechanisms of cell fate decisions. Shortly thereafter he established the Single Cell Omics Center in 2012 to provide access to this empowering technology to the Singapore research community. In October 2014 he moved back to North America, joined JAX, and established the Single Cell Biology Laboratory. He holds an adjunct faculty position in Genetics and Genome Sciences at UConn Health and is faculty in the Genetics and Developmental Biology and the Neuroscience areas of concentration in the UConn Health Graduate School.

In his current lab he continues to exploit advanced tissue mapping technologies and pluripotent stem cell differentiation strategies to understand human biology at single cell resolution. There is a particular emphasis on testing the antagonistic pleiotropy hypothesis of George C. Williams, specifically focusing on understanding features of the human genome that have changed to establish molecular and cellular innovations in embryo implantation unique to primates. Understanding such genomic features and associated biological processes are relevant to female infertility/women’s health, cellular senescence pathways in aging, and tumor-stromal cell interactions, in addition to many other aspects of human biology.

        Paul Robson on orcid        

The overall goals of our laboratory are to understand why the immune system causes autoimmune diseases and to devise methods to predict and treat them. We develop and use mouse strains that provide models for human diseases such as lupus, rheumatoid arthritis and epidermolysis bullosa. We use a combination of genetics, molecular biological and cellular immunological tools to dissect the molecular and cellular processes that cause these diseases. Finally, we study the mechanisms that affect the persistence of antibodies and antibody-based therapeutics. The information gained from all of these approaches is then used to devise possible therapeutic approaches that can be translated to human treatments.

Professor Rosenthal is the Scientific Director of The Jackson Laboratory (Bar Harbor, Maine). She obtained her Ph.D. from Harvard Medical School, where she later directed a biomedical research laboratory, then established and headed the European Molecular Biology Laboratory (EMBL) campus in Rome. She was Founding Director of the Australian Regenerative Medicine Institute at Monash University and founded EMBL Australia as its Scientific Head. Rosenthal is an EMBO member, Fellow of the UK Academy of Medical Sciences and the Australian Academy of Health and Medical Science, is an NH&MRC Australia Fellow, and is the Maxine Groffsky Endowed Chair. She also holds a Chair in Cardiovascular Science at Imperial College London.

Professor Rosenthal is a global leader in the use of targeted mutagenesis in mice to investigate mammalian development, disease and repair. Her research focuses on the role of growth factors, stem cells and the immune system in the resolution of tissue injury for applications to regenerative medicine. Her book, Heart Development and Regeneration, is considered the definitive text in the field. She has received numerous honorary doctorates and prizes, participates on international advisory boards and committees and is a Founding Editor of Disease Models and Mechanisms, Editor-in-Chief of Differentiation and of a new Nature Partner Journal, Regenerative Medicine.

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• Long-COVID and Diversity - Springer Nature has published an article regarding finding ways to study long-COVID, the challenging diversity of symptoms that people experience after recovering from COVID-19, featuring Rosenthal.

Our primary research interest is to understand the genetic basis for immunological tolerance to endogenous proteins. Defects in these mechanisms lead to many debilitating autoimmune diseases, of which type 1 diabetes (T1D) is one of the most serious. In both humans and NOD mice, T1D results when insulin-producing pancreatic ß-cells are destroyed by autoreactive T-cell responses. Thus, insights into the genetic mechanisms responsible for the normal maintenance of immunological tolerance can be gained by identifying the pathogenic basis of T1D in NOD mice.

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Complex biological processes often require in vivo analysis. A fundamental understanding of many biological processes in humans has stemmed from experimental studies in animal models, particularly in laboratory mice. For several decades, our lab has studied the molecular and cellular basis for pathological changes caused by spontaneous mutations that disrupt the development or regulation of the murine hematopoietic and immune systems.  This knowledge has increased our understanding of human disease. Certain mutations result in severe combined immunodeficiency disease (SCID). We have applied the knowledge gained in our studies of SCID mice to optimize them to serve as hosts for human normal and malignant cells and tissues. There is a growing need for animal models to carry out research studies without putting human individuals at risk. We have developed SCID mouse models that support high levels of engraftment with human cells and tissues to overcome these limitations. We have collaborated nationally and internationally with colleagues to develop improved humanized mouse models and optimize the technologies used for engraftment of normal and malignant human cells and tissues. Our research has leveraged these models for translational studies on human hematopoiesis, immunity, autoimmunity, infectious diseases, diabetes, regenerative medicine and cancer.

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Bill's laboratory is currently exploiting new genome-editing technology to study gene function and to model disease in human stem cells.

Bill received his BSc and MSc in Microbiology and Immunology from McGill University in Montreal, Canada. In 1992, he was awarded his Ph.D. in Molecular and Medical Genetics from the University of Toronto where he pioneered gene-trapping technology in mouse embryonic stem (ES) cells. Following his postdoctoral training with Rosa Beddington in Edinburgh, Bill was a group leader at the BBSRC Centre for Genome Research in Edinburgh.

In 1997, Bill took up an appointment as an Assistant Professor at the University of California at Berkeley. Here, his laboratory demonstrated the value of large-scale mutant ES cell resources for gene-based, phenotype-driven screens in mice. With colleagues in the Bay Area, Bill initiated the BayGenomics programme, the first large public gene trap resource.

From 2003 to 2016 Bill led the Mouse Developmental Genetics and ES Cell Mutagenesis teams at the Sanger Center that established a high-throughput pipeline for the production of many thousands of targeted gene mutations in mouse ES cells for EUCOMM (European Conditional Mouse Mutagenesis Program) and KOMP (Knockout Mouse Project) with funding from the European Union and National Institutes of Health . This mutant ES cell resource is the foundation for ongoing efforts by theInternational Mouse Phenotyping Consortium to elucidate the function of all 20,000 genes in the mouse.

Type 2 diabetes is a disease of genes and environment. My laboratory studies the epigenome of human pancreatic islets and their developmental precursor cells. One aim is to use the epigenome as a read-out of effects of type 2 diabetes genetic variants on islet gene expression programs and function. Emerging evidence suggests that normal or disease-predisposing conditions can actually alter a cell's epigenome and lead to abnormal cellular functions. To this end, my lab is investigating how the islet epigenome is altered under different stimulatory and stress conditions. Finally, we are pursuing targeted modification of cells’ epigenomes to facilitate production of bona fide pancreatic islet cells from pluripotent stem cells or other terminally differentiated cells.

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            Michael Stitzel on ORCID           

EndoC-βH1 and Human Islet Genomics

There is an old saying that "pathology is the mother of medicine." Diseases, and more specifically the discipline of studying diseases (pathology), are why we have medicine and biomedical research. Correctly identifying a disease and the various processes each disease undergoes as it develops is the basis of most work done at The Jackson Laboratory.

While Dr. Sundberg semi-retired in 2019, closing his research laboratory that focused on genetic based skin diseases for over 40 years, he continues to work on several grants at The Jackson Laboratory and provides support for collaborators worldwide.

He currently works with Drs. Carol Bult and Dale Begley on the Mouse Models of Human Cancer Database. He provides photomicrographs of spontaneous and experimentally induced mouse cancers and continues to expand the immunohistochemistry spreadsheet with results of new antibodies constantly being optimized by our Histopathology Scientific Service on which he serves as the faculty advisor. Dr. Sundberg also works with Drs. Julia Oh and Anita Voigt on a UV light cutaneous carcinogenesis project.

Dr. Sundberg continues to actively teach the next generation of investigators and pathologists as the PI for an R13 meeting grant, Pathology of Mouse Models of Human Diseases, the 20th annual meeting of which will be held the end of September 2022. As an extension of this annual meeting, Drs. Sundberg, Peter Vogel (St. Jude), and Jerrold Ward (retired, NIH) recently completed a new book, Pathology of Genetically Engineered and Other Mice (Wiley), that will be published in January 2022. In addition, he is on the organizing committee and a regular lecturer in PATHBIO, a European Union international consortium running 3 annual meetings on anatomy and physiology, pathology, and imaging of mouse models throughout Europe. He also continues to sponsor visiting scientists who come to work with him directly to help them interpret results of their research.

Dr. Sundberg’s institutional service continues as the faculty advisor for the Histopathology Sciences Scientific Service. He works with Lesley Bechtold, the service manager, and her staff to support the management and quality control of the service. He regularly reviews slides to assure quality is maintained when new equipment is purchased and put online, often reviews immunohistochemistry slides and creates photomicrographic montages for the service website for new antibodies being optimized, and helps with training as needed.

Fundamental to our interaction with the world, hearing and balance require 'hair cells' in the inner ear to transduce sound, gravity or head movements into electrical impulses relayed to the brain. Our research aims to unravel the developmental mechanisms that give hair cells their characteristic shape to enable perception. Sensory ability arises through a morphogenetic process whereby intricate cytoskeleton polarization produces and orients the stereocilia bundle, the cell compartment where transduction occurs. How multiple levels of polarity are implemented and interconnected during hair cell differentiation remains largely unknown. Understanding morphogenesis in molecular detail will aid the comprehension and potential treatment of hereditary hearing loss. Furthermore, studying cytoskeleton polarization will inform emerging therapies aimed at regenerating hair cells lost to injury or disease during life, where new bundles must be developed de novo.

The past decade has seen a transformational change in our understanding of the human genome and the role it plays in influencing disease risk. Large-­scale projects such as Encyclopedia of DNA Elements (ENCODE) have identified which non-­coding regions correlate with gene regulatory function. Furthermore, the proliferation of genome wide association studies (GWAS) and scans for recent positive selection have identified thousands of loci that influence human health. Taken together, these efforts show the predominant contributors of heritability for complex phenotypes are common polymorphisms that reside within non-­coding regions of the genome. However, despite our progress in mapping cis-­regulatory elements (CREs) and genetic signatures correlated with disease, very few examples exist that mechanistically link genotypic variation to disease risk. This gap in our understanding is based on our inability to understand the sequence context of active CREs and their targets, without which it is difficult to identify single nucleotide variants that directly modulate gene expression. Thus, given the correct technological advances each disease association can become an untapped entry point that has the potential to transform our understanding of disease etiology.

The mission of our research group is to (1) characterize and learn the grammar of cis-regulatory elements, in both mouse and human models, using novel technological approaches such as high-throughput reporter assays and CRISPR based screens of non-coding regions in the genome. (2) Build upon the knowledge from genome wide association studies and leverage this resource of genetic risk to disease in human populations to construct better animal models that precisely reflect disease phenotypes.

The Trowbridge laboratory studies cell fate regulation within the hematopoietic system. Our current focus is on the epigenetic regulation of hematopoietic stem cell (HSC) and progenitor cell lineage commitment in three contexts: (1) normal blood development and maintenance, (2) alterations that occur during the process of aging, and (3) alterations that occur during the process of transformation giving rise to leukemia. Our ultimate goal is to reveal epigenetic patterns and processes that are uniquely deregulated during aging and/or transformation, which can be used to identify novel biomarkers of disease and targets for development of therapeutics.

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Next-generation sequencing technologies have revolutionized biological research and provided unique opportunities to study broad and novel questions about the regulation of gene expression. With these technologies, there has been an exponential increase in the types and amount of high-throughput datasets pertaining to the dynamics of gene expression. These data include gene expression data and genome-wide maps of nucleosome occupancy and open chromatin, epigenetic marks and transcription factor binding sites in cells and organisms under various experimental conditions. In my lab, we develop computational models to take advantage of genomics datasets to study the dynamics and mechanisms of transcriptional gene regulation and identify testable hypotheses for genomic medicine.

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 Duygu Ucar on Google Scholar 

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Our research primarily focuses on decoding the differentiation, activation and regulation of human T cells for optimal immune responses to infectious diseases and their perturbations during chronic diseases or aging. We have contributed to the understanding of how T cell subsets are disrupted during human diseases, especially during HIV infection. Our lab has made several seminal discoveries about the diversity and mechanisms of immune suppression mediated by regulatory T cells and effect or functions of human Th17 cell subsets.

We are a computational cancer biology lab with a research focus on the analysis of cancer genomics data to improve our understanding of cancer biology. We have a specialized research interest in understanding disease progression of brain tumors, and to study the role of extrachromosomal DNA amplifications in cancer. Our group combines wet lab approaches for functional modeling with large datasets and computational methods.

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Acute myeloid leukemia (AML) is an aggressive hematological malignancy that accounts for majority of acute leukemia cases in adults. Despite recent therapeutic advances, AML is still marked by a dismal prognosis. Our laboratory is interested in understanding mechanisms that govern therapy resistance in hematological malignancies by using CRISPR/Cas9 technology and genetically engineered mouse models.

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Dr. Wei received her Ph.D. from University of California, Davis. She continued her postdoctoral training in Massachusetts Institute of Technology, studying Drosophila development and apoptosis. She joined Genome Institute of Singapore in 2002 to start her career track as genomic scientist and established the genome technology platform and genome biology program. She has a strong track record of managing successful, large-scale genome-focused projects. Over the past 20 years, I have built and directed three large-scale HTP sequencing operations and genomic technology innovation centers, with eight years at the Genome Institute of Singapore, six years at the Joint Genome Institute, and now at The Jackson Laboratory. Her core research program includes new sequencing method development and optimization that will enable effective application to transcriptomic, genomic and chromatin analyses.

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Chia-Lin Wei on ORCID