Our research focuses on studying the basic genetics and physiology of mosquitoes with the overarching goal of developing innovative, novel, creative, synthetic biology inspired genetic control technologies for reducing the burden of mosquito-borne diseases on humans. The underlying hypothesis inspiring this work is that the introduction and spread of genes that prevent mosquitoes from transmitting pathogens should, in theory, lead to reduced transmission of these pathogens resulting in reductions of human infections and/or death. To test this hypothesis, we first need a broad understanding of the biology of the mosquito that can be used to develop gene-based strategies for engineering mosquitoes that are resistant to pathogens; secondly, we need to engineer mosquitoes that are resistant to all types of infections; and lastly, we need to develop tools to rapidly “drive” these laboratory developed genes into wild mosquito populations. Together, these aims can conceivably provide a foundation that has the potential to revolutionize vector control of mosquitoes.

Research in the Bennett lab uses integrated biochemical, cellular, and systems level approaches to study cellular stress response pathways and identify new molecular players that sense, evaluate, and propagate cellular stress signals. The overall goal of our research is to leverage these stress response pathways to protect against age-dependent tissue decline.

It's an exciting time at the Bier Lab! We have been forging ahead with great energy on our research, focusing on three integrated areas: 1) Active Genetics, a new CRISPR based methodology developed in the lab that can be used to create gene-drive elements to combat vector borne diseases and to aid in large-scale combinatorial genome engineering, 2) Developmental Patterning, analyzing the mechanisms by which morphogen gradients that initiate patterning are linked to morphogenesis of embryonic and adult structures in fruit flies, and 3) Human Disease Mechanisms, using fruit flies to model human disease such as those caused by barrier disruptive toxins produced by bacteria causing anthrax and cholera.

In an effort to tap into the naturally occurring genetic “selection experiment” that has been underway since the origin of the vertebrate limb, our lab studies the Lesser Egyptian Jerboa, Jaculus jaculus, as a new experimental system. The goal of our research program is to capitalize on each of the jerboa limb novelties as a means to explore the broader and profoundly important relationship between gene regulatory landscapes and phenotypic malleability.

Our lab is interested in understanding how the replicated genome is accurately segregated during cell division. In particular, the lab has dedicated significant effort towards understanding how dynamic coupling between kinetochores and spindle microtubules is achieved and how this coupling is integrated with regulatory mechanisms ensuring accuracy in chromosome segregation. The work on this topic has led the lab into new areas including chemical biology approaches targeting cell division processes, control of cell cycle progression both prior to and during mitosis, pathways for spindle assembly, and linking understanding of cell division mechanisms to cancer cell aneuploidy.

A central question in regenerative biology is how stem cells coordinate decisions to promote proper organ formation. We apply chemical genetics, high spatial resolution metabolomics, and molecular biology to uncover novel signaling pathways during development. We do this work in plant roots, which are excellent models for understanding stem cell behavior. In roots, the full developmental trajectory is optically accessible, genetically tractable, and amenable to high-throughput phenotyping. Additionally, the molecular principles governing many signaling processes are conserved between plants and animals, with implications across agriculture and medicine. Ongoing work is leading to the discovery of new signaling molecules that regulate stem cell decisions.

We are specifically focused on the early secretory pathway, where two organelles, the ER and the Golgi stack, form a ‘synapse-like’ interface that is conserved across taxa. This junction functions as an ‘assembly line’, in which macromolecules (e.g. proteins and lipids) that are manufactured in the ER are shipped to the Golgi, and then processed and distributed to multiple locations within as well as outside of the cell. Our goal is to understand the mechanisms that establish the ER-Golgi interface and enable efficient processing and sorting of cargo within this space. We pursue a ‘bottom-up’ approach in which we purify individual components to homogeneity and probe them in a model membrane environment, seeking out the minimal components and mechanisms needed to reconstitute morphology and function. We complement this approach with super-resolution and electron microscopy, genetic perturbations and functional assays. Through this dual strategy, we hope to elucidate the principles by which the ER-Golgi interface is formed and maintained to execute its many critical cellular functions.

Because plants are sessile, they respond to changes in their environment by altering their growth and development. This plasticity is mediated to a large extent by a group of small molecules called the plant hormones, including auxin, which has been implicated in virtually every stage of plant growth and development. Auxin can elicit different cellular responses depending on the context and is active at a very broad range of concentrations, again depending on the context. The major goal of the Estelle lab is to understand how a simple molecule can mediate such a complex set of cellular responses. We use two genetically tractable plants for our studies; Arabidopsis thaliana and Physcomitrium patens. Our previous work demonstrated that auxin response depends on the rapid degradation of transcriptional repressors called the Aux/IAA proteins through the action of a ubiquitin protein ligase or E3 called SCF TIR1. We are now focusing on how the co-receptor complex is regulated in different tissues and in various environmental conditions. Our work over the last decade has shown that auxin response is highly regulated with overlapping pathways and multiple regulatory loops. As a first step, we want to describe the entire auxin response pathway at the RNA and protein level, as it responds to defined stimuli such as abiotic and biotic stresses. Our ultimate goal is to understand the systems that mediate growth at the level of the organism.

Our lab aims to identify new therapeutic opportunities for the deadliest cancers by merging two disciplines, computational medicine and cancer immunology, to find where tumors are vulnerable and how they can be controlled therapeutically by the immune system. In particular, we are interested in an immune cell type that has not been well-studied, called the B cell. Our goal is to identify and develop therapeutic strategies that leverage B cells to disarm tumor cells and provide long-term protection against cancer activity.

Our research interests are centered on the interface between cell and cancer biology. Our work is focused on mechanistic approaches to dissect the molecular machinery that controls cell division and development, and how variation in the cell division machinery between cell types can be exploited to engineer chemotherapeutic strategies. A parallel focus has been the development of high-content imaging-based screening approaches, which we are employing to dissect mitotic pathways in different human cell types and functionally profile genes specifically required for morphogenesis during embryonic development.

In order to understand the links that connect the genome to neural function, my lab focuses on naturally occurring differences between species. We use the insect visual system as a model, which provides access to diverse brains and nervous systems that have been shaped by a range of requirements, such as expanded color vision in butterflies or improved motion vision in house flies. This approach enables us to understand the rules that are used to build and modify a biological system that can receive input from the world, think, and respond. Our lab is, at the core, a Drosophila lab, taking full advantage of our extensive knowledge of the fly visual system and the panoply of genetic and imaging tools available there, while focusing on uncovering specific genetic changes that make other species different. We work on butterflies, mosquitoes, and house flies, with each species exhibiting unique visual system characteristics.

We strive to understand how the system of the microtubule cytoskeleton and its associated transport machinery works at molecular, cellular, and organismal scales. We are also investigating how defects in microtubule-based transport are linked to Parkinson's Disease and how viruses can subvert the transport machinery. Eukaryotic cells use microtubule tracks to move cargo over long distances. Our lab is tackling broad questions about how the transport system works. How does the dynein motor work and how is it regulated? How does the transport system work? Why do perturbations to the transport machinery cause disease?

Our laboratory’s research is directed at the signal transduction mechanisms and pathways that mediate resistance to environmental (“abiotic”) stresses in plants, in particular responses to elevated CO2, drought, salinity stress, and heavy metal stress. Our research is elucidating the molecular and cell biological stress-induced signal transduction cascades in higher plant cells, examining the chain of events by which plant cells respond to elevated CO2, the drought stress hormone abscisic acid and salinity stress to mount specific resistance and adaptation responses. We have developed and adapted interdisciplinary and systems biological approaches to guard cells, which control water loss and CO2 intake in plants and which have become a key model system for understanding dynamic cellular signal transduction and ion channel functions in plants. A second effort in the lab focuses on identifying genes that mediate salt (sodium) stress resistance and heavy metal uptake and detoxification in plants. Our research into heavy metal stress led to the parallel discovery of the genes encoding the central heavy metal detoxification enzymes in plants, phytochelatin synthases.

Most of our studies are aimed at understanding how mesodermal derivatives commit to the hematopoietic fates during development. We are also interested in understanding the ontogeny of immunity in the zebrafish embryo. Fertilization occurs externally in zebrafish, and the resulting embryos are autonomous from the beginning. Early embryos placed into solutions containing high bacterial titres are extremely resistant to infection. We are examining the components of this early immunity, with the goals of identifying the effectors of innate immunity and developing models of bacterial, protozoan, and helminth infection.

Neurons are exquisitely polarized cells with axons and dendrites that send and receive information. Neuronal activity depends on the localization of proteins, organelles, and vesicles to right place at the right time. The Wildonger laboratory aims to understand how functional neurons are built through the activity of molecular motors and microtubules. We capitalize on the strengths of a fruit fly model to precisely manipulate endogenous protein function in vivo and to image neurons live in intact animals.

Our research is currently divided into two areas: Biological invasions, and Pollination Services. The introduction of species into new environments has increasingly become an economically costly and environmentally destructive phenomenon. Our research on invasions primarily encompasses the following questions: (i) What factors control susceptibility to invasion? (ii) When and why do invasion impacts change in magnitude over time? (iii) To what extent can native species assemblages recover following experimental invader removal?

Our research group designs microbial systems to test outstanding hypotheses in ecology and evolution. Currently our research program includes studies on viral speciation, viral evolvability, and microbiome-host interactions.

The Rennison Lab studies the processes involved in the evolution and maintenance of biodiversity. Our projects involve both controlled lab or field experiments and surveys of wild fish populations. We utilize methods from the fields of genomics, ecology and evolution.

We study evolutionary potential - how stochastic, genetic, and environmental variation is filtered through development and physiology to produce phenotypic variation and how evolutionary forces shape that process. Some research questions and projects in the lab are: Why can’t different species mate and produce viable offspring? How do rules for morphogenesis evolve? How much variation is there in morphogenesis in hypervariable species? How do essential genetic networks originate? What are the different contributions of gene duplication and cis-regulation to the process? Construction and optimization of a synthetic biology system for measuring transcription factor-DNA interactions. Development of a culture system for continuous lifetime monitoring and environmental manipulation of nematode growth, development, and gene expression. Mechanistic dissection of phenotypic variation in a well-understood signal transduction network. Does our understanding of genetic networks extend beyond lab strains?

The Daugherty lab studies how organisms have evolved to detect and neutralize pathogens, and the strategies that pathogens take to overcome those host defenses. Combining computational and experimental approaches, we are particularly interested in genes engaged in rapidly evolving host-pathogen “arms races” in order to understand the causes and consequences of genetic innovation on susceptibility to infection. The majority of current projects in the lab focus on human immunity to circulating and emerging viruses, where we aim to discover novel mechanisms of host antiviral immunity and viral counter-strategies, and to understand how viral and host diversity shape the ability of viruses to “jump” into humans and spread throughout the human population. We also have projects investigating horizontal gene transfer between bacteria and animals, bacteria-bacteriophage conflicts, genetic innovation in invertebrates, and any other cool evolutionary systems that we run across.

WE STUDY THE COMPLEXITY OF MICROBIAL LIFE USING SIMPLIFIED MICROBIAL COMMUNITIES. Microbes rarely live alone. In the ocean, the soil, and the human body, microbes live within complex, multi-species communities. Yet, due to their complexity, it is often extremely difficult to understand how these communities work. To address this challenge, our lab has taken the approach of using simplified microbial communities as model systems.The goal of our work is to understand the basic mechanisms that are at play within microbial communities, such as those that drive species interactions, and to identify general principles of community formation.Our model system of choice is cheese. We are now working to capitalize on this experimental system to identify molecular mechanisms that are responsible for the formation of a microbial community, and to better understand what happens when this process goes wrong.As a result of our work in this simplified system, we aim to provide the scientific community with hypotheses, tools, and strategies for understanding and manipulating more complex microbial communities.

The goal of our lab is to understand how network architecture governs the dynamics and function of regulatory responses in the context of stresses, aging, or diseases. We develop and use novel microfluidics and imaging technologies to quantitatively track the dynamics of molecular processes in single living cells and construct computational models to describe and predict cellular behaviors. In particular, our current work focuses on:(1) decoding the dynamics of stress responses; (2) probing the causes of cellular aging; and (3) quantifying the heterogeneity in cancer cells.

We study how movement and mechanics give rise to function in biology, from the molecular motors that interact with our DNA to the contraction and expansion of the muscles in our heart. We are accepting students from all backgrounds, with the only requirements being a quantitative mindset and a motivation to learn. Our lab has three tracks that address biomechanical questions on different scales: Using DNA origami to study protein-DNA interactions (single molecule biophysics). Integrating molecular motors and DNA origami to build synthetic muscles (synthetic biology). Using single-cell spatial transcriptome profiling to create mechanical maps of the heart (cardiac biology).

We are interested in understanding both cellular and molecular mechanisms underlying the regulation of immune activation and immune suppression, two distinct and yet complementary activities of the immune system. Specifically, our lab focuses on identifying miRNAs crucial for mediating Treg cell biology in healthy and diseased mice and elucidating the molecular and cellular mechanisms by which Treg cells employ to control type I inflammation. Ultimately, we hope to gain insight into the complex biology of these cells, including the maintenance of immunological tolerance to “self” and the regulation of immune responses to pathogens, commensals, and tumors. *Recruiting new students will be contingent on if we take a rotation student this year.

With the long-term goal of understanding how mRNA decay is regulated in gene expression and disease, our lab focuses on dissecting the human cellular mRNA decay machineries. Some of the ongoing projects in this line of research include understanding the regulation of ARE-mediated mRNA decay, elucidating the mechanism behind nonsense-mediated decay, establishing the role of the deadenylases in the ARE- and nonsense-mediated decay pathways, and testing the importance of hDcp1 and hDcp2 proteins in mRNA decapping and decay.

The focus of the lab is to utilize cryo-EM structural biology techniques to decipher the biological complexity characterized by protein assemblies involved in genetic regulation. We are interested in understanding how proteins recognize and alter chromatin structure in order to perform diverse gene regulatory functions. We wish to harness the information we learn through structural biology in order to understand the complex roles proteins play in human diseases, and to ultimately translate our findings from the lab into therapeutic approaches.

We are using cutting edge approaches to bridge the gap between studies of individual molecules, gene regulatory elements such as enhancers, insulators and promoters, mRNA and proteins versus collections of molecules. We are using multi-scale approaches that we integrate across spatial and temporal scales to understand how interactions among these factors combine to determine the physiology of the cell. Currently we are focusing on introducing these new approaches to the study of molecular and physical mechanisms that underpin hematopoiesis in young and aging organisms. We are interested in addressing these problems using single-cell imaging but in the context of live tissue such as the thymus and lymph node.

Our lab focuses on understanding the functional plasticity of the endoplasmic reticulum (ER), especially during cellular responses to developmental stages, new environmental stresses, or other cellular insults. We are specifically interested in two major areas: (1) How are increased demands for ER functions in response to cellular stress and insults recognized and lead to production of those necessary functions, and (2) How is the ER divided in the cell cycle?

MicroRNAs and other types of non-coding RNAs have emerged as key regulators of gene expression, and errors in pathways controlled by these RNAs have been linked to numerous human diseases, including cancer, heart ailments and neurological disorders. Our lab focuses on understanding how regulatory RNAs are expressed and function in the context of normal organismal development, during aging, and in response to stressful conditions. The nematode C. elegans is our primary research model for studying the role of regulatory RNAs and discovering conserved pathways relevant to human health and disease

Our research focuses on the discovery of the phage nucleus and spindle and antibiotic discovery and mechanism of action. Our goals are to identify and characterize the major families of dynamic cytoskeletal proteins that exist in bacteria, to determine the various functions that they perform, and to understand how these polymers are regulated spatially and temporally by other factors within the cell. We specializes in using genetics and cell biology to study the function and in vivo assembly dynamics of cytoskeletal polymers in many different species of prokaryotes, including E. coli, Bacillus subtillis, B. megaterium, B. thuringiensis, Mycobacterium smegmatis, and Pseudomonas species. Our studies have led to the discovery of new types of cytoskeletal structures involved in DNA segregation in bacteria (Pogliano 2008), including a new family of tubulins (Larsen et al. 2007) and a new family of actins (Becker et al. 2006).

Our research is organized around three key themes: Cellular organization and dynamics: Using the framework of cellular organization and dynamics, we seek to understand what are the design principles of bacterial cells. We are also interested in understanding how the outcomes of interspecies microbial interactions are determined. Finally, we turn to chemical Cell Biology to ask how secreted metabolites and antibiotics affect bacterial cells. We take a multidisciplinary approach to our studies, using the tools of genetics, cell biology, proteomics, biochemistry, and we have recently added analytical chemistry to our toolkit.

My lab is interested in understanding how microbial toxins modulate host-microbe metabolism to promote pathogen transmission during infection. We use animal (mouse and rabbit) models of disease coupled with bacterial and host genetics to study the molecular mechanisms of toxin-mediated pathogen growth and transmission. We are currently investigating how cholera toxin-induced disease modulates intestinal metabolism to confer a fitness advantage to Vibrio cholerae during infection. Current projects in the lab include understanding how cholera toxin and other toxins modulate the gut microbiota during disease. We are also interested in understanding how these processes enhance the transmission of the pathogen during disease. Our research may shed light into the development of novel and cost-effective therapeutics for treating and preventing infectious diseases.

Nearly every cell in the human body has the capacity to detect a viral threat, sounding an alarm and recruiting potent antiviral factors and cells that are crucial for determining the course of disease. Nearly every human-adapted virus, in turn, has the capacity to suppress this response and grow unseen by the alarms that protect us from most pathogenic threats. Nevertheless, the body invariably recognizes viral infection in a subset of infected cells. What defines these rare, critical events? Do they represent unique instances of the host overcoming viral antagonism? Do they instead represent failures on the part of the virus, perhaps an inevitable consequence of a rapidly dividing, rapidly mutating, population? The Russell lab uses a multifaceted approach, including single-cell transcriptomics, saturating mutational analysis and highly-parallel genetic screens in order to define this critical interface.

Our laboratory has three primary research interests, one concerned with transcriptional and metabolic regulation in bacteria, a second with transport protein evolution, and a third with the recently identified process of transposon-mediated directed mutation.

We are interested in the problem of organelle homeostasis, using peroxisomes as the model organelle. Our studies on peroxisome homeostasis examine how peroxisomes are assembled (biogenesis) and destroyed (turnover or pexophagy), as well as the coordination of these two processes within cells. We are also interested in the role of peroxisome biogenesis and turnover in disease states.

We study cellular recycling processes in cancer cells, including autophagy and mitophagy. In particular, we are interested in how cancer cells can adapt when recycling processes are altered. We use multi-disciplinary cell biology and molecular biology techniques including genome-wide CRISRR/Cas9 editing, super resolution microscopy, optogenetics, and biochemistry to study autophagy in cancer models including cultured cell lines, patient and mouse derived 3D-organoids, and genetically engineered mouse models. The goal of our work is to identify compensatory mechanisms of autophagy-mediated degradation in order to design better targeted therapies to decrease tumor relapse and increase cancer patient survival.​

The Villa Lab develops tools to observe macromolecular complexes in their natural environment, the cell. Our ultimate goal is to unveil the structural dynamics of these complexes while they go about their everyday life. We combine cell biology and electron microscopy to generate data, and we use image processing and physical modeling to understand these data.

Our laboratory studies cellular and molecular aspects of immune responses during acute and chronic viral infections to determine general principles of antiviral immunity, immune-evasion, persistence and pathogenesis. The ultimate goal is to generate fundamental knowledge on immune-regulation that could help modulating immune responses to prevent or treat infectious diseases and may also have implications for other immune-related illnesses.

Our lab studies how populations of neurons coordinate their activity to implement computations. Specifically, we want to answer the question – What are the features of neural population activity that are important for understanding the dynamics of behavior? We approach this problem with two, parallel approaches: 1) New data analysis tools to help us understand and visualize evolving neural dynamics. 2) New theoretical frameworks for understanding the computational significance of these statistical descriptions. We engage in both of these approaches in close collaboration with experimentalists, theorists, and data scientists and a people-centric, collaborative environment is a big part of our lab culture.

The Banghart Lab seeks to understand how neuromodulators shape goal-oriented behavior and nociception in the mammalian central nervous system. Our multidisciplinary approach relies on electrophysiological, optical and behavioral methods along with in-house development of molecular tools for monitoring and manipulating neurochemical signaling in the brain. We are particularly interested in neuropeptides, which are specifically expressed in distinct cell types that also release GABA or glutamate. Despite their abundance and striking, evolutionarily conserved expression patterns, the physiological roles of most neuropeptides in the brain are largely unknown. To reveal when, where and how neuropeptides modulate neural circuits, we employ contemporary genetically-targeted neuroanatomical methods, whole-cell electrophysiology, two-photon imaging and rodent behavioral analysis, often in conjunction with optogenetic and chemical-genetic perturbations. To facilitate these efforts, we also develop novel molecular tools for observing and manipulating neuromodulatory activity with an emphasis on photoactivatable (caged) neurotransmitters, optical sensors and genetically-targeted pharmacological probes.

We investigate open problems in computational neuroscience — especially concerning synaptic plasticity, memory consolidation, continual learning, representational geometry and efficient coding — using tools from theoretical physics, applied mathematics, machine learning and data science. We examine recordings of neural activity, develop targeted data analysis methods, and build theoretical frameworks to shed light on the mechanisms of biological computation. The main goal of our research is to understand learning and memory under resource constraints in the biological brain, which performs highly non-trivial functions using noisy and severely limited components such as neurons and synapses. By constructing normative mathematical models of brain circuits, which can be tested on experimental data, we attempt to clarify how these limitations are overcome and uncover the underlying computational principles.

My lab’s interests are in the early development of epidermal and neuronal tissues, and in the responses of epidermal and neuronal cells to damage. We are studying epidermal (skin) development as a model for epithelial morphogenesis in the nematode worm Caenorhabditis elegans. We are particularly interested in axon regeneration, epidermal wound healing responses, the extracellular matrix and epidermal cell shape change, and eph signaling and the role of the neuronal substrate in epidermal enclosure.

Glia comprise at least half of the cells in the adult central nervous system (CNS) where they serve as essential regulators of most functions including development, synapse formation, neuronal survival, and disease. Glial cell dysfunction has been implicated in an array of neurological disorders such as Multiple Sclerosis, Alzheimer’s disease, and brain malignancies. Yet our understanding of the development of glial cells and their functions remains to be fully explored.

The laboratory is interested in dissecting the transcriptional regulatory mechanisms controlling glial cell specification during CNS development and during glioma formation. Understanding how gene regulation is coordinated through chromatin conformations, long-range enhancer interactions, and site-specific transcription factors to influence biological phenomena remains a fundamental question that has critical implications for development, physiology, and disease. We are focused on exploring these relationships and how these processes intersect with glioma tumorigenesis

Our laboratory is focused on two problems in neurobiology: (1) Active sensing, where we are delineating the brainstem circuitry that coordinates orofacial motor actions, e.g., sniffing, licking, head bobbing, and whisking, into behaviors. (2) Blood flow in the brain, for which we connect measurements of the topology of the vasculature with neuronal control of flow dynamics from the level of large-scale vascular networks down to single microvessels. Our efforts in both areas involve a broad range of approaches together with the opportunity to develop new tools.

Our laboratories study questions about learning and memory with an emphasis on one of the core systems for memory, which includes the hippocampus and entorhinal cortex. In humans, these brain regions are known to be the basis for declarative memory – the form of memory that we are aware of and can recollect when being asked. In addition, the hippocampus and associated brain regions are also critically important for perceiving space and for navigating in familiar and new environments. While tremendous progress has been made in identifying cellular, molecular, and neural circuits for learning, memory, and navigation, our understanding of the computations that the brain performs to support these functions are incompletely understood. Our laboratories focus on identifying these biological computations and we are also interested in how multiple brain regions cooperatively engage in memory-related function.

Pekkurnaz Lab research focuses on the molecular principles of metabolic homeostasis in the nervous system. By studying the interplay between neuronal metabolism and mitochondrial functions across cell classes, we aim to reveal fundamental insights into the mechanisms that regulate cellular bioenergetics and pinpoint the underlying causes of energy impairments that lead to neurological diseases.

Investigation of the development of neuronal excitability led to the discovery that calcium-dependent embryonic electrical activity rapidly and reversibly reconfigures the transmitters and matching postsynaptic transmitter receptors that neurons express. Activity modulates the transcriptional code for transmitter specification. Both sensory and motor stimuli reprogram neurotransmitter identity, resulting in transmitter switches in young and adult nervous systems. Transmitter switching often converts excitatory neurons to inhibitory ones, or vice versa – a form of plasticity that is distinct from changes in synaptic weights and synapse number. The changes in brain biochemistry during transmitter switching cause changes in behavior that can be beneficial, enhancing learning, or detrimental, contributing to neurological and psychiatric disorders. We study the plasticity of transmitters, specifically in its application in PTSD, autism, drug abuse, and motor control.

The driving force of my lab is to find answers to such questions as: Is the pattern of glomerular activity evoked by a given odor related to the detection of this odor? How is the olfactory information represented and processed in the brain? How is olfactory valence represented in the brain? How is this representation modulated to meet the demands of different internal physiological states? The long-term goal of my laboratory is to elucidate the mechanism of olfaction. Our current research activities aim to identify specific neural circuits underlying olfactory behaviors, investigate how different physiological states of an organism modulate the function of olfactory circuits, and establish causality between neural plasticity in specific neuron populations and olfactory behaviors.

Our nervous system is made of many types of neurons wired into complex circuits, which underlie all our behavior. The Zou lab studies the fundamental molecular signaling and cellular mechanisms of axon guidance and synapse formation and how disruption of these normal processes may lead to developmental disorders, such as autism. We also study how neural circuits respond to and recover from traumatic injury, in the hope to promote their repair and return of function.