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Our research group utilizes the nematode C. elegans to investigate germ cell immortality: mechanisms that allow germ cells remain eternally youthful as they are transmitted from one generation to the next. We also study how telomerase functions at chromosome termini, as well as the consequences of telomere dysfunction.


Laminar organization of neurons in cerebral cortex is critical for normal brain function. Two distinct cellular events guarantee the emergence of laminar organization– coordinated sequence of neuronal migration, and generation of radial glial cells that supports neurogenesis and neuronal migration. Our goal is to understand the cellular and molecular mechanisms underlying neuronal migration and layer formation in the mammalian cerebral cortex. Towards this goal, we are studying the following three related questions: 1. What are the signals that regulate the establishment, development and differentiation of radial glial cells, a key substrate for neuronal migration and a source of new neurons in cerebral cortex?2. What are the signals for neuronal migration that determine how neurons reach their appropriate positions in the developing cerebral cortex?3. What are the specific cell-cell adhesion related mechanisms that determine how neurons migrate and coalesce into distinct layers in the developing cerebral cortex?


Building a functioning brain requires an elaborate network of interactions between neurons and glia. We use mouse genetics, primary cell culture, quantitative proteomics, molecular biology, and super resolution microscopy to study glial cells during brain development. We are particularly interested in how astrocytes acquire their complex morphology and communicate with neighboring astrocytes, neurons, and oligodendrocytes. Furthermore, we are investigating how glial dysfunction drives the pathogenesis of brain disorders such as autism, schizophrenia, and leukodystrophy.


Blood vessel formation in cancer and development; use mouse culture (stem cell derived vessels) and in vivo models (embryos and tumors); genetic, cell and molecular biological tools; how do vessels assemble and pattern?, dynamic image analysis.


Dr. Belger’s research focuses on studies of the cortical circuits underlying attention and executive function in the human brain, as well as the breakdown in these functions in neuropsychiatric and neurodevelopment disorders such as schizophrenia and autism. Her research also examines changes in cortical circuits and their physiological properties in individuals at high risk for psychotic disorders. Dr. Belger combines functional magnetic resonance imaging, electrophysiological scalp recording, experimental psychology and neuropsychological assessment techniques to explore the behavioral and neurophysiological dimensions of higher order executive functions. Her most recent research projects have begun focusing on electrophysiological abnormalities in young autistic children and individuals at high risk for schizophrenia.


The Brenman lab studies how a universal energy and stress sensor, AMP-activated protein kinase (AMPK) regulates cellular function and signaling. AMPK is proposed to be a therapeutic target for Type 2 diabetes and Metabolic syndrome (obesity, insulin resistance, cardiovascular disease). In addition, AMPK can be activated by LKB1, a known human tumor suppressor. Thus AMPK signaling is not only relevant to diabetes but also cancer. We are interested in molecular genetic and biochemical approaches to understand how AMPK contributes to neurodegeneration, metabolism/cardiac disease and cancer.


How do networks of cells synchronize behaviors across differing spatial and temporal scales? This fundamental aspect of cellular dynamics is broadly relevant to understanding many biological systems in which the coherence of electrical or chemical signals is required for multicellular patterning or organ function. Our group’s primary research interests are related to understanding the cellular and microenvironmental conditions that are required to support the biorhythmic behavior of the system of cells that natively control heart rate, cardiac pacemaker cells. We utilize a variety of techniques including computational modeling, next generation sequencing, in vivo genetic manipulation, super-resolution imaging, and direct physiological recording to investigate the developmental processes that assemble the hearts pacemaking complex. The ultimate goals of these studies is to determine how the pacemaker cell lineage is patterned in the embryo, build strategies towards fabricating this cell type for therapeutic purposes, and identify vulnerabilities that may lead to pacemaker cell pathologies in humans.


The immune system of severely burned patients becomes extremely suppressed after injury. An overwhelming number of patients die from wound infection and sepsis. However, we are unable to graft these patients with skin from other donors as their immune system is still able to reject the graft efficiently. Our inability to cover the wound site leaves the patients further open to bacterial and fungal infections. Our laboratory investigates the translational immune mechanisms for these devastating consequences of burn within mouse models and burn patients. Focuses in the lab include 1) investigation of innate molecule control of both the innate and adaptive immune systems after burn injury, 2) Role of innate signaling to Damage Associated Molecular Patterns in Immune Dysfunction after burn / inhalational injury,focusing on mTOR-mediated Immunomodulation 3) Using NRF2/KEAP1-Targeted Therapy to Prevent Pneumonitis and Immune Dysfunction After Radiation or Combined Burn-Radiation Injury and 4) Investigating sex-specific disparities in Immune Dysfunction after trauma / transplantation. ​


Gene targeting and state-of-the-art phenotyping methods are used to elucidate the reproductive and cardiovascular roles of the adrenomedullin system and to characterize the novel GPCR-signaling mechanism of Adm’s receptor and RAMP’s.


Males and females differ in their prelevance, treatment, and survival to a diverse set of human disease states. This is exemplified cardiovascular disease, a disease that takes more lives than all forms of cancer combined. In cardiac disease, women almost uniformly fare far worse than men: as of 2007 one woman dying for cardiovascular disease in the US every minute. Our lab focuses on sex disparities in development and disease. For these studies, we use a highly integrated approach that incorporates developmental, genetic, proteomic, biochemical and molecular-based studies in mouse and stem cells. Recent advances by our past students (presently at Harvard, John Hopkins and NIH) include studies that define the cellular and molecular events that lead to cardiac septation, those that explore cardiac interaction networks as determinants of transcriptional specificity, the mechanism and function of cardiac transcriptional repression networks, and the regulatory networks of cardiac sexual dimorphism. Our lab has opening for rotation and PhDs to study these rapidly emerging topics.


My lab studies how cell proliferation is controlled during animal development, with a focus on the genetic and epigenetic mechanisms that regulate DNA replication and gene expression throughout the cell cycle. Many of the genes and signaling pathways that we study are frequently mutated in human cancers. Our current research efforts are divided into three areas:  1) Plasticity of cell cycle control during development  2) Histone mRNA biosynthesis and nuclear body function  3) Epigenetic control of genome replication and function.


Dr. Gilmore’s research group is applying state-of–the-art magnetic resonance imaging and image analysis techniques to study human brain development in 0-6 year olds.  Approaches include structural, diffusion tensor, and resting state functional imaging, with a focus on cortical gray and white matter development and its relationship to cognitive development.  Studies include normally developing children, twins, and children at high risk for schizophrenia and bipolar illness.  We also study the contributions of genetic and environmental risk factors to early brain development in humans.  A developing collaborative project with Flavio Frohlich, PhD will use imaging to study white and gray matter development in ferrets and its relationship with cortical oscillatory network development.


During development transcriptional and posttranscriptional networks are coordinately regulated to drive organ maturation, tissue formation, and cell fate. Interestingly, more than 90% of the human genes undergo alternative splicing, a posttranscriptional mechanism that explains how one gene can give rise to multiple protein isoforms. Heart and skeletal muscle are two of the tissues where the most tissue specific splicing takes place raising the question of how developmental stage- and tissue-specific splicing influence protein function and how this regulation occurs. In my lab we are interested on two exciting aspects of this broad question: i) how alternative splicing of trafficking and membrane remodeling genes contributes to muscle development, structure, and function, ii) the coupling between epigenetics and alternative splicing in postnatal heart development.


The Gladden lab studies how cell adhesion and cell polarity are intertwined in normal tissue development and how these pathways are altered in diseases such as cancer. We use a combination of 3D cell culture, mouse models and protein biochemistry to study how cell polarity and adhesion regulate tissue organization. Our work focuses on the interplay between cell adhesion and cell polarity proteins at the adherens junction and how these proteins regulate tissue organization. We concentrate on the development of the endometrium epithelium in the female reproductive tract and the cell biology of endometrial cancer.


We address fundamental issues in cell and developmental biology, issues such as how cells move to specific positions, how the orientations of cell divisions are determined, how the mitotic spindle is positioned in cells, and how cells respond to cell signaling – for example Wnt signaling, which is important in development and in cancer biology. We are committed to applying whatever methods are required to answer important questions. As a result, we use diverse methods, including methods of cell biology, developmental biology, forward and reverse genetics including RNAi, biochemistry, biophysics, mathematical and computational modeling and simulations, molecular biology, and live microscopy of cells and of the dynamic components of the cytoskeleton – microfilaments, microtubules, and motor proteins. Most experiments in the lab use C. elegans embryos, and we have also used Drosophila and Xenopus recently. C. elegans is valuable as a model system because of the possibility of combining the diverse techniques above to answer a wide array of interesting questions. We also have a project underway to develop a new model system for studying how cellular and developmental mechanisms evolve, using little-studied organisms called water bears. Rotating graduate students learn to master existing techniques, and students who join the lab typically grow their rotation projects into larger, long term projects, and/or develop creative, new projects.


The Good Laboratory is focused on the cellular and molecular mechanisms involved in the pathogenesis of a devastating intestinal disease primarily affecting premature infants called necrotizing enterocolitis (NEC). The long-term goal of the Good Lab is to understand the signaling pathways regulating the uncontrolled immune response in NEC and how these responses can be prevented through dietary modifications or targeted intestinal epithelial therapies. Her basic and translational research utilizes a bench-to-bedside approach with multiple cutting-edge techniques. In her pre-clinical studies, their team utilizes a humanized neonatal mouse model of NEC to understand the signaling pathways and immune cell responses involved in NEC development. Specifically, the laboratory interrogates ways to modulate the immune response, epithelial cell and stem cell regeneration as well as early microbial colonization during NEC. In the clinical component of her research program, Dr. Good leads a large multi-center NEC biorepository for the dedicated pursuit of molecular indicators of disease and to gain greater pathophysiologic insights during NEC in humans. Dr. Good also developed a premature infant intestine-on-a-chip model to study NEC and provide a personalized medicine approach to test new therapeutics. Her laboratory is currently funded with multiple NIH R01 grants and has previously received K08 and R03 funding as well as awards from the March of Dimes, the Gerber Foundation and the NEC Society.


The Gordon lab is brand new to UNC, and studies stem cell and stem cell niche biology in the model organism C. elegans. The germ line stem cells make the gametes, which make the next generation of worms. These cells are therefore at the nexus of development, genetics, and evolution. We will be getting started with projects pertaining to evolutionary comparative gene expression in the stem cells and stem cell niche and niche development. The techniques we use include molecular biology, CRISPR/Cas9-mediated genome editing, worm genetics, and microscopy.


The human placenta is the first organ to develop after fertilization and is the least studied! We hope to change this by using a multidisciplinary approach. From iPSC-derived trophoblasts in culture to mouse models and human placenta tissue, the Placental Cell Biology Group at NIEHS answers fundamental questions about placenta cell and developmental biology. Our lab uses a range of microscopy (cryo-EM, fluorescence), recombinant protein production, and -omics techniques. The goal of our research is to understand how autophagy controls placenta development, differentiation, and function.


The Neurotoxicology Group examines the role of microglia interactions with neurons and the associated immune-mediated responses in brain development and aging as they relate to the initiation of brain damage, the progression of cell death, and subsequent repair/regenerative capabilities.  We have an interest in the neuroimmune response with regards to neurodegenerative diseases such as, Alzheimer’s disease.


The lab focus is to understand the mechanism of gene-environment interactions by examining the genetic basis of epigenetic response to nutrition and environmental toxicants. The long-term goal is to identify and characterize genetic (naturally occurring and induced) and environmental (toxicant and nutritional) causes of disruption of DNA methylation patterns during development and to determine their role in disease. The primary focus is on DNA methylation patterns during germ cell and early embryonic development during critical windows of epigenetic reprogramming.


The Jacox Lab aims to improve patient care and outcomes in oral health. This goal takes shape via several tracks of interdisciplinary human studies:

-A primary focus of the lab has been on outcomes of jaw surgery patients, who suffer from Dentofacial Disharmonies (DFD). Patients with DFD have severe skeletal disproportions with underbites or open bites, necessitating orthodontics and jaw surgery for full correction. Roughly 80% of our patients with DFD exhibit speech distortions, compared to 5% of the general population, which negatively impact their self-confidence and quality of life. Despite patients pursuing invasive surgery, it is unknown whether jaw surgery is palliative for articulation errors. We are using ultrasound, audio and video imaging to explore the mechanism of articulation errors among patients with DFD. Furthermore, our lab is conducting a longitudinal study of DFD patients to determine if jaw surgery improves speech distortions, in collaboration with oral surgeons, linguistics and speech pathology.

-An additional focus of our lab has been studying use of Animal Assisted Therapy for management of anxiety and pain in dentistry. Dental anxiety effects 21-50% of patients and is associated with poor long-term oral health outcomes and need for urgent care due to dental avoidance. Non-pharmacological behavior interventions like dog therapy holds promise for reducing pain and anxiety perception for patients, and therefore improving dental experiences and promoting improved health outcomes. The lab is conducting a randomized controlled trial to evaluate best practices for canine therapy in pediatric dentistry, in collaboration with pediatric dentists, a psychology professor whose expertise is anxiety, and the UNC Biobehavioral Lab.

-As part of the COVID-19 research response, we are studying FDA-approved antiseptic mouth rinses for their ability to limit salivary viral infectivity to reduce risk of SARS-CoV-2 transmission. If an oral rinse is found to be efficacious at inactivating the SARS-CoV-2 virus, it could be a valuable preventative measure in settings where masks are removed, such as dental care, social settings, eating out, or work presentations. This study is conducted in collaboration with leading virologists and infectious disease experts at UNC.


Hormones influence virtually every aspect of plant growth and development. My lab is examining the molecular mechanisms controlling the biosynthesis and signal transduction of the phytohormones cytokinin and ethylene, and the roles that these hormones play in various aspects of development. We employ genetic, molecular, biochemical, and genomic approaches using the model species Arabidopsis to elucidate these pathways.


Congenital heart diseases are one of the most common birth defects in humans, and these arise from developmental defects during embryogenesis.  Many of these diseases have a genetic component, but they might also be affected by environmental factors such as mechanical forces. The Liu Lab combines genetics, molecular and cell biology to study cardiac development and function, focusing on the molecular mechanisms that link mechanical forces and genetic factors to the morphogenesis of the heart.  Our studies using zebrafish as a model system serve as the basic foundation to address the key questions in cardiac development and function, and could provide novel therapeutic interventions for cardiac diseases.


My research goals are to identify the mechanisms by which environmental factors regulate smooth muscle cell phenotype and to define the transcriptional pathways that regulate SMC-specific gene expression.


My research philosophy is summed up by a quote from Nobelist Albert Szent-Gyorgyi: “Discovery is to see what everybody has seen and to think what nobody has thought.” My lab studies the molecular and physical mechanisms of cell shape change during cytokinesis and tissue biogenesis during development. Specifically, we are defining how cells ensure proper alignment and sliding of cytoskeletal filaments, and determining the shape of the cell throughout division. To do so, we combine developmental biology, cell biology, biochemistry, and quantitative image analysis.


The Magnuson Lab works in three areas – (i) Novel approaches to allelic series of genomic modifications in mammals, (ii)Mammalian polycomb-group complexes and development, (iii) Mammalian Swi/Snf chromatin remodeling complexes


My research focuses on molecular mechanisms of mammalian nervous system development. We investigate mechanisms by which developing neurons migrate to the neocortex and form connections.


We are interested in the mechanisms by which histone protein synthesis is coupled to DNA replication, both in mammalian cell cycle and during early embryogenesis in Drosophila, Xenopus and sea urchins.


The research in our laboratory focuses on epigenetics and RNA processing. In particular, we are interested in the roles of small ribonucleoproteins (RNPs) and histone post-translational modifications in the regulation of eukaryotic gene expression.  There are two main projects in the lab. (1) We have created a comprehensive genetic platform for histone gene replacement that — for the first time in any multicellular eukaryote — allows us to directly determine the extent to which histone post-translational modifications contribute to cell growth and development. (2) We study an RNP assembly factor (called Survival Motor Neuron, SMN) and its role in neuromuscular development and a genetic disease called Spinal Muscular Atrophy (SMA). Current work is aimed at a molecular understanding of SMN’s function in spliceosomal snRNP assembly and its dysfunction in SMA pathophysiology.


The McCauley Lab is interested in how the food we eat changes our physiology. Rare, nutrient sensing cells in the intestine called enteroendocrine cells secrete hormones in response to environmental cues that orchestrate systemic metabolism. How these cells regulate their neighbors in the gut is not well understood. We use mouse models which lack enteroendocrine cells and human pluripotent stem cell derived intestinal organoids to discover new roles for these master metabolic cells in the regulation of intestinal physiology and function. Enteroendocrine cells are dysregulated in inflammatory bowel disease, type 2 diabetes, and obesity, and loss of enteroendocrine cells results in malabsorptive diarrhea with poor survival. Our research has the potential to improve human health for a wide segment of the global population.


Research in the lab focuses on how a single genome gives rise to a variety of cell types and body parts during development. We use Drosophila as an experimental system to investigate (1) how transcription factors access DNA to regulate complex patterns of gene expression, and (2) how post-translational modification of histones contributes to maintenance of gene expression programs over time. We combine genomic approaches (e.g. CUT&RUN/ChIP, FAIRE/ATAC followed by high-throughput sequencing) with Drosophila genetics and transgenesis to address both of these questions.


The Morris lab leverages flexible mouse models of hard to treat cancers of the pancreas and liver to identify how cancer drivers perturb evolutionarily selected developmental programs and how such programs may be re-normalized. We focus on (1) the relationship between tumor suppressor pathways and the epigenetic determinants of cell plasticity, (2) evolutionary routes unleashed by specific tumor suppressor loss, and (3) how diversification at both the epigenetic and genomic level contribute to cancer development and therapeutic response.


Understanding how cells communicate and co-ordinate during development is a universal question in biology. My lab studies the cell to cell signaling systems that control plant stem cell production.  Plants contain discrete populations of self-renewing stem cells that give rise to the diverse differentiated cell types found throughout the plant.  Stem cell function is therefore ultimately responsible for the aesthetic and economic benefits plants provide us. Stem cell maintenance is controlled by overlapping receptor kinases that sense peptide ligands. Receptor kinase pathways also integrate with hormone signaling in a complex manner to modulate stem cell function.  My lab uses multiple approaches to dissect these networks including; genetics, genomics, CRISPR/Cas9 genome editing, live tissue imaging, and cell biological and biochemical methods.  This integrated approach allows us to gain an understanding of the different levels at which regulatory networks act and how they contribute to changes in form and function during evolution.


Modern Technologies from next-gen sequencing to high resolution imaging have advanced our knowledge of kidney development, function, and disease. We are among the pioneers utilizing techniques such as CHIP-seq, RNA-seq, modern genome editing, and imaging to understand how regulatory programs control progenitor populations during kidney development. Our goal is to understand how these programs contribute to progenitor specification and maintenance, and how they are altered during disease and aging. Our ultimate goal is translational applications of our research to develop new therapeutics and regenerative strategies.


Non-Mendelian genetics including, meiotic drive, parent-of-orifin effects and allelic exclusion.


Our research focuses on the genetic and cellular mechanisms that underlie how prenatal exposure to alcohol and other drugs, such as cannabinoids, disrupt normal brain development. We use a wide variety of molecular and cell biology tools including RNA-seq (whole transcriptomic profiling), mouse transgenics, and confocal imaging to understand how drugs alter cell signaling pathways and transcriptional regulation in development. Our work also studies key regulatory pathways, such as Sonic hedgehog (Shh) and other primary cilia-mediated signals, during normal and aberrant embryonic development.


Cell adhesion, cytoskeletal regulation and Wnt signaling in development and cancer
The Peifer lab works at the interface between cell, developmental, and cancer biology, focusing on the epithelial tissues that form the basic architectural unit of our bodies and of those of other animals. We explore how the machinery mediating cell adhesion, cytoskeletal regulation and Wnt signaling regulates cell fate and tissue architecture in development and disease. We take a multidisciplinary approach, spanning genetics, cutting edge cell biology including super-resolution microscopy, biochemistry and computational approaches. We use the fruit fly Drosophila as an animal model and combine that with work in cultured normal and colorectal cancer cells. Possible thesis projects include exploring how connections between cell junctions and the cytoskeleton are remodeled to allow cells to change shape and move without tearing tissues apart or exploring how the tumor suppressor protein APC assembles a multi-protein machine that negatively regulates Wnt signaling and how this goes wrong in colorectal tumors. I am a hands on-mentor with an open-door policy and my office is in the lab. I value and advocate for diversity. Our lab has a strong record of training PhD students and postdocs who move on to success in diverse science-related careers. Our lab is funded by a long-standing NIH grant that extends to July 2021, and just received a good score for renewal. To learn more about or research, our recent publications, our team and our alumni check out the lab website at: https://proxy.qualtrics.com/proxy/?url=http%3A%2F%2Fpeiferlab.web.unc.edu%2F&token=1rPNJvHEEfhAAiwkSviuOG0Fg8%2ByN3Q3GMob1A2GJwM%3D


It is estimated that less than 2% of the human genome codes for a functional protein.  Scattered throughout the rest of the genome are regulatory regions that can exert control over genes hundreds of thousands of base pairs away through the formation of DNA loops.  These loops regulate virtually all biological functions but play an especially critical role in cellular differentiation and human development. While this phenomenon has been known for thirty years or more, only a handful of such loops have been functionally characterized.  In our lab we use a combination of cutting edge genomics (in situ Hi-C, ATAC-seq, ChIP-seq), proteomics, genome editing (CRISPR/Cas), and bioinformatics to characterize and functionally interrogate dynamic DNA looping during monocyte differentiation.  We study this process both in both healthy cells and in the context of rheumatoid arthritis and our findings have broad implications for both cell biology as well as the diagnosis and treatment of human disease.


Many diseases of the kidney remain poorly understood. My research program spans a range of disciplines (e.g., genetics, cell biology, immunology) and experimental approaches (e.g., microscopy, molecular biology, biochemistry, and model organisms—Drosophila and zebrafish) to answer fundamental questions regarding the genetic and cellular basis of kidney function and disease. We are also developing novel assays to study autoimmune diseases of the kidney, with the goal of facilitating patient diagnosis and treatment. By applying modern tools to long-standing problems, we hope to translate our research findings to improved patient outcomes.


Our laboratory is interested in developing innovative approaches to regenerate or repair an injured heart. Our goal is to understand the molecular basis of cardiomyocyte specification and maturation and apply this knowledge to improve efficiency and clinical applicability of cellular reprogramming in heart disease. To achieve these goals, we utilize in vivo modeling of cardiac disease in the mouse, including myocardial infarction (MI), cardiac hypertrophy, chronic heart failure and congenital heart disease (CHD). In addition, we take advantage of traditional mouse genetics, cell and molecular biology, biochemistry and newly developed reprogramming technologies (iPSC and iCM) to investigate the fundamental events underlying the progression of various cardiovascular diseases as well as to discover the basic mechanisms of cell reprogramming.


Regulation of plant development:  We use techniques of genetics, molecular biology, microscopy, physiology, and biochemistry to study how endogenous developmental programs and exogenous signals cooperate to determine plant form.  The model plant Arabidopsis thaliana has numerous technical advantages that allow rapid experimental progress.  We focus on how the plant hormone auxin acts in several different developmental contexts.  Among questions of current interest are i) how auxin regulates patterning in embryos and ovules, ii) how light modifies auxin response, iii) how feedback loops affect kinetics or patterning of auxin response, iv) how flower opening and pollination are regulated, and v) whether natural variation in flower development affects rates of self-pollination vs. outcrossing.


The research in our lab is centered on understanding the mechanisms and principles of movement at the cellular level. Cytoskeletal filaments – composed of actin and microtubules – serve as a structural scaffolding that gives cells the ability to divide, crawl, and change their shape.  Our lab uses a combination of cell biological, biochemical, functional genomic, and  high resolution imaging techniques to study cytoskeletal dynamics and how they contribute to cellular motion.


The Shiau Lab is integrating in vivo imaging, genetics, genome editing, functional genomics, bioinformatics, and cell biology to uncover and understand innate immune functions in development and disease. From single genes to individual cells to whole organism, we are using the vertebrate zebrafish model to reveal and connect mechanisms at multiple scales. Of particular interest are 1) the genetic regulation of macrophage activation to prevent inappropriate inflammatory and autoimmune conditions, and 2) how different tissue-resident macrophages impact vertebrate development and homeostasis particularly in the brain and gut, such as the role of microglia in brain development and animal behavior.


Our laboratory studies the coordination of histone-modifying enzymes in regulating chromatin structure, enhancer activation, and transcription. We utilize mouse genetics and cell culture model systems to study the mechanisms of enhancer activation in neural crest cell epigenetics, craniofacial development, and altered enhancer regulation in cancer. This is accomplished through a variety of techniques including mouse mutagenesis, fluorescent reporters to isolate primary cells of interest, low cell number genomics, and proteomic approaches.


Our primary research interest is to identify the mechanisms that regulate neural circuit organization and function at distinct stages of adult neurogenesis, and to understand how circuit-level information-processing properties are remodeled by the integration of new neurons into existing circuits and how disregulation of this process may contribute to various neurological and mental disorders. Our long-range goals are to translate general principles governing neural network function into directions relevant for understanding neurological and psychiatric diseases. We are addressing these questions using a combination of cutting-edge technologies and approaches, including optogenetics, high-resolution microscopy, in vitro and in vivo electrophysiology, genetic lineage tracing and molecular biology.


We are a lab exploring how variations in the genome change the structure and development of the brain, and in doing so, create risk for neuropsychiatric illness. We study genetic effects on multiple aspects of the human brain, from macroscale phenotypes like gross human brain structure measured with MRI to molecular phenotypes like gene expression and chromatin accessibility measured with genome-sequencing technologies. We also use neural progenitor cells as a modifiable and high fidelity model system to understand how disease-associated variants affect brain development.


The goal of our research is to identify signaling mechanisms that contribute to normal and pathophysiological cell growth in the cardiovascular system.  We study cardiac and vascular development as well as heart failure and atherosclerosis.


With an emphasis on chromatin biology and cancer epigenetics, our group focuses on mechanistic understandings of how chemical modifications of chromatin define distinct patterns of human genome, control gene expression, and regulate cell proliferation versus differentiation during development, and how their deregulations lead to oncogenesis. Multiple on-going projects employ modern biological technologies to: 1) biochemically isolate and characterize novel factors that bind to histone methylation on chromatin, 2) examine the role of epigenetic factors (chromatin-modifying enzymes and chromatin-associated factors) during development and tumorigenesis using mouse knockout models, 3) analyze epigenomic and transcriptome alternation in cancer versus normal cells utilizing next-generation sequencing technologies, 4) identify novel oncogenic or tumor suppressor genes associated with leukemia and lymphoma using shRNA library-based screening. We are also working together with UNC Center of Drug Discovery to develop small-molecule inhibitors for chromatin-associated factors as novel targeted cancer therapies.


Reproductive biology of early mammalian embryogenesis including gametogenesis, fertilization, and preimplantation embryo development. Effects of environmental disrupting chemicals on female reproductive tract development and function, with a focus on epigenetic alterations.


Interest areas: Developmental Biology, Cell Biology, Cancer Biology, Stem Cells, Genetics

PhD programs: Pathobiology & Translational Sciences, Genetics & Molecular Biology, Cell Biology & Physiology, Oral Biology, Biology

Tissue development and homeostasis depend on the precise coordination of self-renewal and differentiation programs. A critical point of regulation of this balance is at the level of cell division. In the Williams lab, we are interested in stratified epithelial development, stem cells, and cancer, with a particular interest in how oriented cell divisions contribute to these processes. Asymmetric cell divisions maintain a stable pool of stem cells that can be used to sustain tissue growth, or mobilized in response to injury. However, dysregulation of this machinery can lead to cancer, particularly in epithelia where tissue turnover is rapid and continuous. Using the mouse epidermis and oral epithelia as model systems, we utilize cell biological, developmental and genetic approaches to study the molecular control of oriented cell divisions and mitotic spindle positioning, and how division orientation impacts cell fate choices in development, homeostasis, injury, and disease.


We employ modern technologies – genomics, proteomics, mouse models, multi-color digital imaging, etc. to study cancer mechanisms. We have made major contributions to our understanding of the tumor suppressor ARF and p53 and the oncoprotein Mdm2.