Faculty Members

Areas: EEB, Micro/Immuno
The Aylward lab is broadly interested in the ecology and evolution of viruses. Hallmark discoveries made over the last ~40 years have underscored the importance of microbes to the planet and shown that global biogeochemical cycles are driven by diverse groups of bacteria, archaea, protists, and their viruses, most of which lack any cultivated representatives. Novel viral lineages continue to be discovered using cultivation-independent methods, and currently a major challenge is understanding the ecology and evolution of these groups, what governs their host range and infection dynamics, and their broader impact on the biosphere. We use a combination of computational and experimental approaches to investigate the phylogenetic, genomic, and metabolic diversity of various viral groups. 

aylward@vt.edu
5092 Derring Hall
(540) 231-8657
 

Area: EEB
Research in the Barrett Lab addresses the influences of soils, climate variability, hydrology and biodiversity on biogeochemical cycling from the scale of microorganisms to regional landscapes. Topics that I am interested in are:

• Transformation and transport of carbon, nitrogen and phosphorus across terrestrial and aquatic ecosystems.
• Controls over spatial distribution of soil biota
• Response of soil biota to climate variability
• Soil community composition and ecosystem functioning
• Carbon sequestration in managed ecosystems

jebarre@vt.edu
2026 Derring Hall
(540) 231-3827

Area: EEB
In the Belden Lab at Virginia Tech we primarily study community ecology, with a focus on understanding how complex communities influence disease dynamics in natural systems.  Most of our work has focused on addressing these questions in the symbiotic microbial communities that reside on amphibian skin and in communities of freshwater trematode parasites.  However, our work on symbiotic microbes has expanded in recent years to include some new and exciting systems, including song birds, honey bees and wheat.

belden@vt.edu
4088 Derring Hall
(540) 231-2505

kabretz@vt.edu
2082-C Derring Hall
(540) 231-0790

Area: EEB
Dr. Brown's research covers a fairly broad range of themes, but the majority of the work conducted in his lab would fall under the heading Community Ecology in Aquatic Systems.  His lab's research also tends to revolve around experimental tests of ecological theory and relies heavily on field experimentation.  

Six main themes that characterize research either currently underway or recently completed in the Brown Lab:  

• Keystone mutualisms in streams
• The metacommunity concept and stream ecosystems
• The influence of habitat heterogeneity on community stability
• Isolated Wetlands:  Ecology and Conservation
• Community Assembly:  Priority effects and disturbance
• Effects of perturbations on aquatic communities

brown51@vt.edu
2030 Derring Hall
(540) 231-2065

Area: MCDCB
Current research in my laboratory focuses on adaptor protein trafficking within the endolysosomal system, autophagy, and macropinocytosis. These pathways are essential for cellular homeostasis, as they coordinate cargo recognition, vesicle transport, and degradation. Our goal is to define the molecular mechanisms by which adaptor proteins regulate cargo sorting, vesicle tethering, and fusion events across these trafficking routes. We employ biochemical and biophysical approaches to elucidate the structural and functional basis of adaptor protein interactions, identify regulatory binding interfaces, and characterize membrane insertion processes at molecular to atomic resolution. These studies provide mechanistic insight into how adaptor proteins integrate lipid signals with protein trafficking and how their dysregulation contributes to human disease.

capellut@vt.edu
263-C Steger Hall
(540) 231-0974

Area: EEB

My work lies at the intersection of freshwater ecosystem science and data science and I get excited about lots of different questions exploring anthropogenic effects on inland waters. I am broadly interested in nutrient and carbon cycling in freshwater ecosystems and the feedbacks that occur between aquatic biogeochemical cycles and plankton food webs. I also am interested in how local communities value and manage their water resources, which has implications for water quality. I particularly like working in interdisciplinary, collaborative teams to solve water challenges. Check out the lab’s Publications page to explore our most recent work or my Google Scholar profile.

At Virginia Tech, my research has expanded into near-term ecological forecasting and I serve as the Co-Director of the Virginia Tech Center for Ecosystem Forecasting. In collaboration with computer scientists, environmental engineers, decision scientists, and water utilities, my lab group integrates high-frequency sensor data and ecosystem models to generate daily water quality forecasts that predict a suite of freshwater ecosystem services for lakes and reservoirs across the U.S.  I study how managers use forecasts of future conditions to control hypoxia and algal blooms, which in turn alters biogeochemical cycling and greenhouse gas dynamics. For more information, see our project website on the Virginia Reservoirs LTREB program.

Finally, a major goal of my lab is to advance undergraduate training in environmental data science. I am the Founder and Director of Macrosystems EDDIE (Environmental Data-Driven Inquiry & Exploration), an NSF-supported program to develop teaching modules that train undergraduates ecological modeling, forecasting, and computational literacy. By integrating messy, high-frequency sensor datasets into undergraduate curricula, students simultaneously learn the core concepts of ecology while developing the quantitative skill sets needed to conduct the next generation of environmental research.

cayelan@vt.edu
2027 Derring Hall
(540) 231-8938
 

Area: MCDCB
Cells are highly dynamic: gazillions of dynamic processes are happening in a cell at any moment in order for the cell to sense, respond and adapt to their environments, to move around, to develop and reproduce, to evolve, and even to maintain homeostasis.

We build theoretical and computational models to investigate complex biological dynamics at the molecular, cellular and cell population levels, and to understand how they mediate biological functions. To build models that are biologically relevant and impactful, we work in close collaboration with experimental groups.

chenjing@vt.edu
5100 Derring Hall
(540) 231-1359

Area: MCDCB
Maintenance of a correct number of chromosomes is necessary for organismal development and survival. Animal cells maintain a correct diploid chromosome number by equally segregating their DNA (chromosomes) into two daughter cells at each division cycle. When chromosome segregation does not occur correctly, daughter cells with abnormal chromosome numbers are produced. Abnormal chromosome numbers are a distinctive feature of cancer cells and such chromosome number changes are believed to contribute to cancer progression. Therefore, understanding the mechanisms leading to inaccurate chromosome segregation is critical for understanding the process of carcinogenesis and will be the starting point for the development of diagnosis, prevention, and treatment protocols. Our laboratory uses a combination of live-cell imaging, quantitative microscopy, and protein inhibition to identify the cellular and molecular mechanisms underlying normal and abnormal cell division behaviors. To enhance the breadth and scope of our work, we often collaborate with engineers and mathematical modelers.

cimini@vt.edu
2125 Derring Hall
162-A Steger Hall 
(540) 231-3922

Area: MCDCB
Successful cell division requires distributive segregation of genome copies into daughter cells. Early in division microtubules form a bipolar spindle that aligns replicated chromosomes along the metaphase plate. As sister chromatids begin to segregate apart, a large contractile structure made up of f-actin and non-muscle myosin II assembles along the equatorial cortex of the cell aligned with the division plane. This actomyosin contractile ring is a highly dynamic structure that constricts to physically drive membrane ingression and cell division. We combine cell biology techniques, such as quantitative fluorescence microscopy and genetics, with computational techniques, such as agent-based modeling, to characterize the molecular mechanisms of cell division. We are particularly interested in investigating how chromosome segregation defects in anaphase alter contractile ring composition and dynamics during cytokinesis and abscission. 

dbcortes@vt.edu
162-B Steger Hall
(540) 231-7254

Area: EEB
Most people think of evolution as a very slow and incremental process, but change can also be quick and innovative. This rapid adaptation can help a population dodge extinction, exploit a new niche, or transform its relationship to its environment. We use computer simulations, mathematical models, and evolution experiments with microbes to learn about how these big changes happen.

Adaptive Evolution of Niche Breadth
In an NSF-funded project, we’re examining how rapid evolution and environmental change can come together to drive specialization–a population focusing in on a narrower niche. We hope to understand what features of a species might predict its propensity to narrow, maintain, or even broaden its niche in the face of competing demands from multiple changing environments. See our first publication from this project in Draghi (2021) Am. Nat.

Predicting Evolution with Phenotypic Models
With collaborators in the Marx, Martinez-Gomez, and Dalia labs, we’re fitting data to a model of metabolism in a model bacterium to understand gene interactions, explain the phenotypic bases of fitness, and ultimately predict outcomes of evolution experiments in the lab. See Chou, Delaney, Draghi & Marx (2014) for an early publication on this work.

Evolvability as a mediator of generalist-specialist competition
A species’ niche–its place in an ecosystem–is not fixed, but evolves and responds to change across that species’ community. Evolution of the species and its competitors, prey, predators, parasites, or hosts, all work to dynamically shape the niche, and past evolution provides a historical framing for why a species functions as it does today. We tackle these complex issues with models combining ecology and evolution. In a recent pair of papers, we looked at how intrinsic noise in development can smooth fitness landscapes to allow plastic generalists to flourish, and how environmental noise across a spatial landscape can shape competition between generalists and specialists. We’re continuing to push toward a theoretical understanding of how evolvability differences shape communities and are expanded to test these theories with lab experiments with microbes.

jdraghi@vt.edu
4001 Derring Hall
(540) 231-6802

memori@vt.edu
2082 Derring Hall
(540) 231-9792

jaevans1@vt.edu
2089 Derring Hall
(540) 231-6408

Area: MCDCB
Connecting scientific disciplines to cure cancer
Does the body's internal clock hamper the effectiveness of radiation therapy? 
Finkielstein’s lab studies the molecular clocks that tell cells when it’s time to grow, divide, and die. Cells in our body have a predictable 24-hour cycle of division that is regulated by a mix of genetic and environmental cues, such as exposure to light, temperature, and hormone levels. At around sunset every day, freshly divided daughter cells undergo rigorous review, during which DNA replication is completed and an average of 20,000 daily mutations are repaired.

finkielc@vt.edu
R-3008, Riverside 2
FBRI
(540) 526-2630

Area: EEB
Our lab integrates behavioral studies in the wild with genomic, phenotypic, biomechanical, and biogeographic analyses, to address questions about the evolution of animal behavior, its role in generating morphological diversity, and the origin and persistence of species. Our primary study system is birds in South America.  

valentinagb@vt.edu
4070-C Derring Hall
(540) 231-9867

Area: EEB
The Gray Lab research priorities are focused on addressing questions related to environmental toxicology, primarily using physiological and ecological approaches to examine the impacts of legacy and emerging contaminants (PAHs, POPs, microplastics, nanoplastics, and pharmaceuticals) from anthropogenic influence and assessing their risk to a variety of freshwater and marine organisms.

austindg@vt.edu
3002 Derring Hall
(540) 231-1079

Area: MCDCB
Cell division is a highly orchestrated process. Both daughter cells need to obtain a precise copy of the genetic information and all other cellular material that they need to survive. We want to understand how such a complex event can be reliably executed, despite fluctuations in cellular composition ('noise') and variation in the cell environment. Because cell division is so central to life, much of the regulation is preserved throughout evolution.  We use the unicellular eukaryote Schizosaccharomyces pombe (fission yeast) as a model organism and combine genetic techniques, advanced fluorescence microscopy, proteomics, and computational modeling to explore the mechanisms of reliable cell division.

silke.hauf@vt.edu
385 Steger Hall
(540) 231-7318

Area: EEB
My research program investigates the ecological and evolutionary mechanisms that underlie host susceptibility, pathogen virulence, and transmission. I approach disease ecology from a multi-disciplinary perspective in order to understand how individual physiology, pathogen virulence, social behavior, and environmental context all interact to influence infectious disease dynamics. My current research projects are briefly described below:

1. Social behavior and disease. Social behavior in animals can have profound effects on susceptibility to infectious diseases and their transmission within and between groups. In turn, infected animals often change their behavior in ways that may influence their likelihood of spreading a pathogen.  My lab studies both directions of this relationship- how behavior influences disease (via both exposure and susceptibility), and in turn, how disease alters behavior in transmission-relevant ways.
2. Evolution of pathogen virulence in a novel host. We recently documented the evolution of increasing virulence in a directly-transmitted pathogen of North American house finches - Mycoplasma gallisepticum. This pathogen is a Mollicute (wall-less) bacterium that relies strongly on its host for survival, and therefore would be predicted to cause minimal virulence in order to maximize its own transmission. We are testing whether incomplete host immunity can select for higher virulence in this system by favoring pathogen isolates that are sufficiently virulent to infect and transmit between individuals with some pre-existing immunity.  
3. Causes and consequences of phenotypic immune variation.  My lab studies the intrinsic (hormones, genetics) and extrinsic (temperature, social environment) factors that influence immune function as well as the consequences of immune variation for disease susceptibility and transmission.  In the house finch-Mycoplasma system, the clinical signs of disease are largely caused by the host immune response rather than direct damage by the pathogen.  Thus, non-intuitively, individuals with the strongest immune response may contribute the most to transmission in this system.  More broadly, we are interested in the ecological and evolutionary causes and consequences of immune variation in natural populations.

dana.hawley@vt.edu
363-C Steger Hall
(540) 231-8946

ehogan@vt.edu
2094-D Derring Hall
(540) 231-0045

Area: EEB

We study the chemicals that make up life on earth and how they change in freshwater ecosystems.

What's in the water? Why is it there? How does it change? What does that mean for things that live in the water or the water we drink?

Freshwater ecosystems (streams, wetlands, ponds, rivers, lakes, and reservoirs) provide many important services, including drinking water, fisheries production, pollutant removal, flood control, and recreation. Changes in the environment (for example: storms/droughts, pollution, landscape development, climate change, and flow modifications) can disrupt or enhance the services provided by freshwaters, often through alterations in freshwater ecology (the interactions between living things and their environment).

As freshwater ecosystems expand and contract across landscapes and merge together at confluences, they connect and disconnect different sources of water and chemicals. The chemicals entering water from land and confluences can serve as food resources or pollutants, and thus alter the ecology of freshwater ecosystems. When the living things within freshwaters (algae, bacteria, fungi, plants, and animals) breathe, eat, grow, reproduce, and die, they respond to and change the chemistry of the water around them. 

We study the chemicals that make up life on earth and how they change in freshwater ecosystems. We investigate the connections between freshwater chemistry and ecology using environmental sensors, water chemistry analyses, experiments, and ecosystem models. Our research provides new knowledge about how freshwater ecosystems function as well as how changes in the environment alter freshwater chemistry, ecology, and ecosystem services.

ehotchkiss@vt.edu
2006 Derring Hall
(540) 231-7005

Area: EEB
Research in my lab lies at the intersection of disease ecology, wildlife biology, and conservation. We work to understand the ecological and evolutionary impacts of emerging infectious disease in wildlife communities. We currently have projects focusing on transmission dynamics in multi-host communities, climate effects on disease dynamics, host and pathogen response following introduction, and management solutions for imperiled wildlife.

jrhoyt@vt.edu
363-A Steger Hall
(540) 231-3822

Area: Micro/Immuno
Trillions of bacteria live in the human gut, and so do bacteriophages — viruses that infect bacteria. We work out what these phages do to gut bacterial communities, and we engineer them into precision therapeutics.

Precise: Most interventions act on the gut microbiome broadly. Phages often infect with species to strain-level specificity, so it can target individual bacteria while leaving the rest of the community alone.

Prevalent: Phages are a native part of the gut, present in enormous numbers. What they do to bacterial communities is still largely uncharacterized and represents an area of opportunity for study.

Programmable: A phage can carry genetic cargo, introducing this material to resident gut bacteria during the infection process and turning them into tiny microbial factories.

bhsu@vt.edu
115 Life Sciences I Building
(540) 231-4246

Area: EEB
Research in the Igwe Lab generally focuses on at least one of three topics: Life in Extreme Environments, Microbiome-Based Horticultural and Agricultural Improvements, or Soil Conservation, Remediation, and Regeneration. We use a range of tools from ecology, microbiology, and molecular biology to answer fundamental questions about how organisms exist in otherwise inhospitable habitats and apply that knowledge to improve the health of people and the planet.

aigwe@vt.edu
2028 Derring Hall
(540) 231-9967

Area: MCDCB
The Johnstone Lab focuses on understanding how healthy blood vessels are altered in disease and defining effective pathways to therapeutically target vascular disease. Cardiovascular disease affects over a third of Americans, causing approximately 2,200 deaths per day. In the U.S., 50 percent of cardiovascular disease patients are less than 60 years old, resulting in a need to effectively treat patients for many years to maintain vascular health.

scottrj@vt.edu
Room 2208, Riverside 4
FRBI
(540) 526-2296

Area: MCDCB
How can long non-coding RNAs regulate circadian rhythms without producing a protein!?
We recently identified a novel non-coding transcript, Per2AS, that appears to play an important role in the mammalian circadian clock system. Interestingly, both of our mathematical and experimental analyses demonstrated that Per2AS confers robustness to the system, and regulates the amplitude of circadian rhythms. How does Per2AS regulate robustness and amplitude without producing a protein? What is the function of Per2AS in vivo? Does Per2AS have additional functions other than regulating circadian rhythms?

What makes circadian rhythms in each organ different from each other?
Cell-autonomous circadian clocks drive thousands of rhythmic output genes that, ultimately, produce daily rhythms of many types of physiology and behavior. Interestingly, the number of cycling transcripts is vastly different among mouse tissues, despite the core molecular machinery (i.e., transcription-translation feedback loops) being nearly identical in all the tissues.
 
We are interested in understanding why some tissues are more robust and produce more cycling genes than others. To answer this, we bioinformatically characterized circadian transcriptome datasets in 12 mouse tissues and found that Rorc, one of the core clock genes, may be the key player to determine which tissues are more robust. We are currently using various experimental tools to validate our bioinformatical prediction and to understand how Rorc contributes to the robustness of the tissues.

Is RNA degradation important for high amplitude circadian gene expression?
Circadian RNA expression is essential to ultimately regulate a plethora of downstream rhythmic biochemical, physiological, and behavioral processes. Both transcriptional and posttranscriptional mechanisms are considered important to drive rhythmic RNA expression; however, the extent to which each regulatory process contributes to the rhythmic RNA expression remains controversial. To systematically address this, we monitored RNA dynamics using metabolic RNA labeling technology during a circadian cycle in mouse fibroblasts. We find that rhythmic RNA synthesis is the primary contributor of 24-h RNA rhythms, while rhythmic degradation is more important for 12-h RNA rhythms. These rhythms were predominantly regulated by Bmal1 and/or the core clock mechanism, and the interplay between rhythmic synthesis and degradation has a significant impact in shaping rhythmic RNA expression patterns. Interestingly, core clock RNAs are regulated by multiple rhythmic processes and have the highest amplitude of synthesis and degradation, presumably critical to sustain robust rhythmicity of cell-autonomous circadian rhythms. Our study yields invaluable insights into the temporal dynamics of both 24- and 12-h RNA rhythms in mouse fibroblasts.

skojima@vt.edu
245-D Steger Hall
(540) 231-5196

Area: MCDCB
1. Achromobacter xylosoxidans (Ax) infection

We use collections of clinical Ax isolates obtained from individual patients over the course of chronic infection to investigate how the pathogen adapts within the host.

1. How does Ax develop multidrug resistance? Several longitudinal isolate series show dramatic changes in antibiotic resistance over the course of infection. We use comparative genomics to identify genetic changes associated with the emergence of antibiotic resistance and dissect the molecular mechanisms underlying these changes.
2. How Ax adapt to the host during prolonged infection? Ax virulence changes substantially between isolates collected from early and late stages of infection. Using comparative genomics together with immunological approaches, we identify genetic changes that occur during chronic infection and investigate how these changes affect bacterial virulence, host interactions, and long-term persistence.

2. Develop inhibitors of bacterial phospholipases

Bacterial phospholipases contribute to virulence in a number of important pathogens and represent potential targets for anti-virulence therapy. We use the P. aeruginosa T3SS effector ExoU as a model bacterial phospholipase to identify and develop inhibitors of bacterial phospholipases. Our goal is to develop strategies that interfere with bacterial virulence and pathogenicity without directly targeting bacterial survival.

P. aeruginosa manipulates the host by injecting its T3SS substrates into host cells. The effector ExoU has the strongest impact on host pathology of all Pseudomonas T3SS effector proteins. ExoU has phospholipase A2 activity that disrupts the host cell membrane and promotes inflammation when ExoU is activated inside the host cell. Delaying expression of ExoU can increase the survival of infected mice.  ExoU homologs have been found and validated in a number of bacterial pathogens. Our current efforts include SAR study of ExoU inhibitors identified from molecular docking.

hanhlam@vt.edu
117 Life Sciences I Building
(540) 231-5741

Area: MCDCB
The LaMantia Lab’s work focuses on how neural circuits in the brain develop for distinct human behaviors. In addition, his lab studies how neural stem cells develop into specific cell types in the embryonic as well as adult nervous system. His work has illuminated the earliest causes of multiple profound developmental disorders in children, including research into a complex disorder of brain, heart, and facial developmental disabilities.

anthonysl@vt.edu
FBRI
(540) 526-2208

Area: EEB
Our work incorporates empirical and theoretical approaches to address research questions on the ecology and evolution of infectious diseases. To answer these questions, we draw from the fields of community ecology, population biology, behavioral ecology, epidemiology, and evolution.

We are especially interested in factors that influence pathogen transmission and population impacts. Much of our recent work has focused on understanding how variation among individuals - in susceptibility, infectiousness, and mortality - contributes to disease outbreaks.

To investigate these questions, we work in a number of different systems across taxa.

Our heterogeneity in susceptibility work is primarily in collaboration with Marc Lipsitch, Gabriela Gomes, and Andrew Wargo, where we are using a model system of rainbow trout, as well as data from other empirical systems, to understand how variation among individuals contributes to pathogen outbreaks. We are also trying to understand how vaccines change variance in population susceptibility.

Our heterogeneity in host infection and mortality focuses on the emerging infectious disease, white-nose syndrome, caused by the fungal pathogen Pseudogymnoascus destructans. The disease was first detected in a cave in upstate New York in 2006, and has since caused severe mortality in bat populations across eastern North America. Our research on white-nose syndrome is primarily focused on investigating factors that influence transmission, impacts, and bat community persistence. This work is highly collaborative and we work particularly closely with Joseph Hoyt, Marm Kilpatrick, and Jeff Foster, as well as state partners.

klangwig@vt.edu
363-D Steger Hall
(540) 231-5678

Area: MCDCB
Cancer is a disease of the cell cycle that results in uncontrolled proliferation of cells. In our laboratory, we explore the molecular mechanisms of breast cancer cell cycle regulation by using holistic, mass spectrometry-based systems biology approaches. We develop proteomic technologies for investigating the pathways that enable cancer cells to bypass tightly regulated molecular checkpoints, proliferate in an unrestrained manner, metastasize and hijack normal biological function. Further, we capitalize on the power of our proteomic data to identify novel therapeutic drug-targets, and to develop microfluidic architectures for targeted detection of biomarkers indicative of disease.

malazar@vt.edu
2011 Integrated Life Sciences Building
(540) 231-5077

Area: Micro/Immuno
Our team studies the fundamental processes of innate immune memory and inflammation dynamics related to health and disease. We have pioneered signal-strength and duration dependent innate memory dynamics such as sustained low-grade immune-enhancing inflammation (under repetitive challenges with weak signals, e.g. subclinical endotoxemia; oxidized phospholipids; cholesterol), tolerance with anti-inflammatory immune suppression (under transient strong septic signals); exhaustion with pathogenic inflammation and immune suppression (under repetitive strong septic signals) as well as resolution of monocytes and neutrophils. Our integrated experimental and computational analyses reveal key mechanistic principles of innate immune memory. Our translational studies reveal crucial significance of distinct innate memory dynamics during the pathogenesis of diverse acute and chronic diseases such as sepsis and atherosclerosis.

Low-grade immune-enhancing inflammation memory during the pathogenesis of atherosclerosis Through integrated approaches that combine mechanistic and complementary functional examinations, we characterized monocytes with low-grade inflammatory memory features shared among mice and humans. Mechanistically, we defined the disruption of homeostatic resolution as the fundamental principle for the generation of sustained low-grade inflammation memory. We defined that the unique signaling adaptor TRAM(TICAM2) serves as an indispensable gatekeeper for initiating and sustaining low-grade inflammation memory by disrupting pexophagy. We demonstrated that the persistence of low-grade inflammatory monocytes contributes to the pathogenesis of atherosclerosis.

Innate exhaustion memory during sepsis Innate leukocytes are rewired during sepsis into a prolonged exhaustion state with the paradigm of pathogenic inflammation and immune suppression, which subjects the host to compromised defense to secondary infections as well as elevated risks for multi-organ inflammation and damage. Our group defined exhausted monocytes with the depletion of key metabolic fuel NAD+, initiated by TRAM related molecular circuitries. We first defined that exhausted monocytes can be generated by repetitive challenges with high dose endotoxin. The generation of exhaustion memory is responsible for long-term complications following the initial bout of septic insult.  

Therapeutically, we are interested in developing approaches that can restore cellular homeostasis. We defined that chemical rejuvenation of peroxisome via 4-PBA or genetic deletion of TRAM adaptor can effectively reprogram innate leukocytes into active resolving states, capable of propagating innate homeostasis and reducing inflammatory disease pathogenesis. We identified resolving monocytes and neutrophils characterized by elevated CD200R and reduced TRAM expression in both murine and human systems. We characterized immune-enhancing and less pathogenic inflammatory neutrophils capable of mounting an effective and broad spectrum anti-tumor defense. Translational relevance during the pathogenesis and treatment of atherosclerosis, sepsis, cancer, and related inflammatory diseases are being examined using transgenic animal models as well as human blood samples.

Ongoing studies include biochemical, molecular as well as functional studies of innate immune memory dynamics in response to damage/danger signals with varying strength and duration under the setting of either acute or inflammatory conditions. Key intertwined players such as TRAM, TOLLIP, and IRAK-M are being examined in directing intra-cellular signaling circuitries involved in innate polarization and reprogramming dynamics. Our biochemical analyses reveal Tollip as a homeostatic molecule facilitating autophagy completion through interacting with PIP lipids. Sustained low-grade inflammatory signals disrupt Tollip function and compromises innate homeostasis.

lwli@vt.edu
149 Life Sciences Building I
(540) 231-1433

Area: EEB
Our research focuses on understanding the molecular underpinnings of phenotypic evolution, especially with regard to complex traits. Our main research program takes an organism-centered approach to investigate the evolution of aposematic coloration and extreme toxicity in poison frogs, especially the genus Phyllobates. Integrative approaches are essential for a rigorous understanding of biological phenomena. Our research draws from a variety of computational and experimental perspectives across the biological sciences, including genomics, population genetics, systematics, developmental biology, molecular physiology, high-throughput biological imaging, and genome editing. Therefore, an important portion of our research program is focused on developing tools and resources to establish poison frogs as a model system in integrative biology.

rmarquezp@vt.edu
3100 Derring Hall
(540) 231-9917

Area: EEB
Research in the McGlothlin Lab focuses on the evolution of complex phenotypes. We are interested both in how selection shapes integrated groups of traits and in the genetic and physiological mechanisms that underlie such trait groups. We tackle these problems using both empirical and theoretical approaches and incorporate ideas and techniques from diverse fields, including evolutionary genetics, behavioral ecology, and physiology.

joelmcg@vt.edu
4038 Derring Hall
(540) 231-0046

Area: Micro/Immuno
The assembly and functions of type IV pili in the Gram-positive anaerobic pathogenic bacterium, Clostridium perfringens.

Identifying the cellular mechanisms responsible for secretion of toxins by C. perfringens.

The interactions of C. perfringens with the host immune system.  Specifically, the molecular mechanisms that allow the bacteria to kill, and avoid being killed by, phagocytic cells of the immune system, macrophages and neutrophils.

melville@vt.edu
5038 Derring Hall
(540) 231-1441

The Massey Herbarium at Virginia Tech seamlessly integrates leading-edge multi-disciplinary research to solve complex issues of local to global relevance involving the southeastern flora with preparing the next generation of scientists and educating the public in diverse ways.

Dr. Metzgar came to VT after working at the University of Alaska Herbarium for ten years. His research has long focused on fern systematics, including his doctoral research on the circumboreal fern genus Cryptogramma.

metzgar@vt.edu
3006 Derring Hall
(540) 231-6768

Area: EEB
Dr. Mims’s research investigates how species’ traits and environmental attributes interact to influence community and population structure of aquatic organisms. Her research integrates the fields of population, community, and landscape ecology, and she uses a suite of approaches including population and landscape genetics, spatially explicit individual-based models, traits-based inference, species distribution models, and multivariate statistical tools. The overarching goal of her research is to uncover, understand, and predict differential response of aquatic species to a changing landscape and climate. Dr. Mims works to bridge fundamental work in freshwater population and community ecology with applied conservation and management needs.

Areas of research interest in the Mims Lab include: 1) developing and testing traits-based approaches and multispecies assessments to prioritize regional management and conservation of freshwater species; 2) assessing species’ vulnerability to climate change across levels of biological organization, from genes to communities; 3) evaluating risk and response of aquatic organisms to climate-driven spatiotemporal changes in intermittent aquatic habitat in lotic and lentic systems.

mims@vt.edu
263-E Steger Hall
(540) 231-6799

Area: EEB
How do animals respond to changes in their physical and social environments, what are the mechanisms mediating the behavioral and physiological responses, and what are the consequences for the individual and population?

These are the types of questions we address in our research. As such, our work crosses traditional disciplinary lines to achieve a more complete understanding of animal function. We try to identify important questions and then utilize appropriate methods to answer them. Our general premise is that one must study, or at least appreciate, animals in their natural environments if one is to truly understand how they work. A strength of our research is the combination of field based observations of classical naturalists with the rigorous experimentation and techniques of modern biologists.

itmoore@vt.edu
4100 Derring Hall
(540) 231-2112

Area: EEB
Projects in the Moss Lab span two major themes with theoretical foundations in evolutionary biology, ecology, and behavior. 

Reproduction in Changing Environments 
With global environments changing at an unprecedented rate, biologists are grappling to understand how natural populations will respond over demographic and evolutionary timescales. While much of this work has focused on organismal performance at environmental extremes, broadscale changes over space and time are also likely to trigger cascading effects on social and reproductive systems via bottom-up effects on individual behavior and physiology. Past and ongoing work in the Moss lab aims to uncover these links by combining long-term monitoring and rigorous experimental approaches. 

Evolution of Parental Care
In many species of animals, successful reproduction hinges on parental care of offspring. Parental behaviors are incredibly diverse in nature and range simple egg brooding to the coordinated provisioning of hungry, begging offspring. What differentiates a doting parent from a neglectful mother or filial cannibal? Past and ongoing work in the Moss Lab aims to uncover the extrinsic (e.g., social and environmental cues) and intrinsic (e.g., physiological, neural, and molecular changes) mechanisms that underpin parental behavior across contexts and understand how behavioral plasticity may facilitate or constrain the evolutionary diversification of care.

jbmoss@vt.edu
4036 Derring hall
(540) 231-9819

Area: Micro/Immuno
We work on the structure, synthesis, and hydrolysis of the peptidoglycan wall components of vegetative cells and endospores. Studies utilize the model Gram-positive bacterium Bacillus subtilis and the pathogens Bacillus anthracis and Clostridium difficile. Molecular genetic techniques are used to identify and manipulate the genes encoding the enzymes that polymerize and hydrolyze the peptidoglycan. Biochemical methods are used to examine the activities of these proteins and the peptidoglycan structural alterations associated with genetic and phenotypic changes. Potential applications of this research are in antibiotic design and in spore-killing for decontamination procedures.

dpopham@vt.edu
5016-B Derring Hall
(540) 231-2529

ruppia@vt.edu
2034 Derring Hall
(540) 231-5360

Area: Micro/Immuno
Bacterial motility and chemotaxis

1. Sensing of environmental signals
2. Two-component signal transduction
3. The speed-variable flagellar motor
4. Flagellotropic phage infection
5. Function of type IV pili in symbiosis
6. Tumor-targeting Salmonella

bscharf@vt.edu
113 Life Sciences I Building
(540) 231-0757

Area: Micro/Immuno
We use an integrated approach to study molecular mechanisms underlying signal transduction in bacteria. We are particularly interested in non-canonical systems that modulate virulence gene expression in the opportunistic pathogen Pseudomonas aeruginosa. Examples include the ExsA-ExsC-ExsD-ExsE signaling cascade, which uses a partner-switching mechanism to regulate expression of the type secretion system in response to host-cell contact. Using the GacS/GacA system as a model we are also deeply interested uncovering the mechanisms underlying crosstalk between signaling histidine kinases in multikinase networks.

fschubot@vt.edu
5002 Derring Hall
(540) 231-2393

Area: EEB
Our research seeks to understand how neural and behavioral processes – and the environmental and developmental factors that impact those processes – contribute to animals’ survival and reproductive success.

This work is relevant to understanding the proximate basis of adaptive and dysfunctional behavior, and is also relevant to understanding the evolution of the brain and behavior.

Our current work focuses on three key areas:

EARLY LIFE CONDITIONS
Environmental conditions early in development are known to impact learning through organizational effects on the brain. In the extreme case, developmental challenges such malnutrition and exposure to pathogens or toxins can impair learning throughout life. On-going work in the Sewall lab is examining how environmental contaminants such as lead and mercury, postnatal nutrition, and early life infection may impair learning by interfering with postnatal brain development. Song learning in birds provides an excellent opportunity to pursue these questions because this form of learning occurs during a critical period early in life and is underpinned by neuronal growth within a specific neural circuit.

SOCIAL DYNAMICS
Sociality is argued to select for intelligence in animals, because navigating social relationships requires superior cognition and associated brain mechanisms. Although evolutionary change underlies some specialization for sociality, within species correlations between group size, cognition, and neuroplasticity suggest that these traits can also change during an animal’s lifetime. However, surprisingly few studies have examined how individuals’ cognitive performance and underlying neuroplasticity change as a function of social conditions. Understanding how animals respond to changing social conditions includes assessing such plasticity, which requires evaluating developmental plasticity (aka organizational effects), life-long flexibility, and the physiological mechanisms that modulate traits.

URBANIZATION
Human habitat disturbance is now recognized as impacting the phenotypes of wild animals and is a particular concern for wild birds. Though some species are threatened by human habitat disturbance, many animals adjust their behavior and physiology through phenotypic plasticity to cope with environmental change. Such plasticity is often sufficient to permit animals to adjust to changing environmental conditions and behavior can be the first means by which animals respond to ecological change in an effort to maintain homeostasis.

Endocrine mechanisms are a major link between organisms’ perceptions of environmental conditions and behavioral and physiological responses and, thus, play a central role in mediating phenotypic plasticity. There is an urgent need to understand the endocrine mechanisms that permit animals to cope with changing environments because understanding the proximate basis of phenotypic adjustments to habitat disturbance will shed light on why some species persist and others decline when faced with a changing environment. Reciprocally, determining how novel environmental conditions alter endocrine phenotypes provides insight into the function and evolution of these mechanisms.

Our lab studies song sparrows living along a rural-urban gradient around Blacksburg, VA. We have found that urban song sparrows are more aggressive than their rural counterparts and that stress hormones (glucocorticoids) and activation of the social behavior network in the brain, but not testosterone, may underpin this behavioral difference.

ksewall@vt.edu
4092-C Derring Hall
(540) 231-5617

tad@vt.edu
2094-C Derring Hall
(540) 231-2774

Area: MCDCB
Investigating pathological changes to intercellular communication

What are the critical mechanisms regulating cell communication in health and disease?
Events that stress the heart, including ischemia and viral infections, disrupt communication between heart muscle cells, creating underlying abnormalities that generate irregular heart rhythms. James Smyth and his team focus on electrical connections between heart muscle cells, called gap junctions, formed by the protein connexin 43 (Cx43). In essentially all forms of cardiomyopathy, loss or altered regulation of Cx43 occurs and results in impaired electrical conduction and contributes to sudden cardiac death. The team's over-arching goal is to identify critical therapeutic targets to restore or preserve normal electrical coupling in diseased hearts and prevent the arrhythmias of sudden cardiac death.

The lab is also extending this work to cancer, where different forms of Cx43 and its functions contribute to altered cell signaling, invasive behavior, and therapeutic resistance.

As molecular virologists, Smyth and his team also study how respiratory viruses such as adenovirus and coronavirus affect the heart and replicate themselves. The team is investigating specifically how viruses reprogram the cell at the molecular level to harness this information therapeutically for myocarditis and beyond.

Using a combination of RNA biology, biochemical assays, live-cell imaging, and super-resolution microscopy, the Smyth Lab aims to uncover new therapeutic strategies to restore electrical integrity in the injured and infected heart.

smythj@vtc.vt.edu
R-2116, Riverside 2
FBRI
(540) 526-2238

Area: Micro/Immuno
The Stevens Lab works in the general field of molecular microbiology with an emphasis on bacterial environmental sensing and gene regulation.  The majority of the research projects focus on the phenomenon of bacterial quorum sensing, a mechanism whereby bacterial cells communicate with one another through the use of small molecules called autoinducers.  By understanding this mode of bacterial gene regulation, methods to manipulate it in ways beneficial to society may be discovered.  Historically, the group has studied quorum sensing in the symbiotic bioluminescent bacterium Vibrio fischeri.  Current work in the laboratory, using modern molecular-based techniques, involves studies about quorum sensing in the corn pathogen (Pantoea stewartii) and a foodborne human pathogen (Vibrio parahaemolyticus).

ams@vt.edu
5036 Derring Hall
(540) 231-9378

Area: EEB, MCDCB
We are a computational biology lab that develops and applies machine learning methods to perform various kinds of phylogenetic inference. Accurate estimation of historic relationships between populations or species remains one of the most formidable tasks of contemporary evolutionary biology. Phylogenetic trees that delineate these relationships serve as a cornerstone structure for almost any basic research leveraging evolutionary information. That is to say, in addition to helping to reconstruct the Tree of Life, phylogenetic analyses can help researchers track the evolution of gene families, trace viral outbreaks, perform ancestral state reconstruction, conduct “phylogenetically-aware” drug design and vaccine development, trace the evolution of human spoken languages, and numerous other basic as well as practical applications.

asu@vt.edu
5076 Derring Hall
(540) 231-9927

Area: MCDCB, Micro
The Tholl Lab studies the formation and biological functions of small molecules or "info"-chemicals in organism-environment interactions. Current research is focused on the 1) Genomics, metabolism, and functions of volatile "messengers" in plant roots and the rhizosphere; 2) Biochemical evolution, chemical ecology and genetic engineering of insect pheromones.

tholl@vt.edu
409 Latham Hall
(540) 231-4567

Area: EEB
Ecosystem: We study the forest and freshwater ecosystems upon which society depends.

Dynamics: We model how ecosystems change over time in response to land-use, climate change, atmospheric deposition, and management.  

Forecasting: We predict the future of ecosystems by combining observations and ecosystem models using statistical techniques.

rqthomas@vt.edu
315-B Steger Hall
(540) 231-7608

Area: MCDCB
My lab focuses on two chemical defense systems that protect plants from attack by generalist herbivores.  Crucifer plants produce glucosinolates, nontoxic glycosides, that are bioactivated when herbivores attack the plant.  We humans recognize these bioactivated compounds as the sharp flavor components of arugula, horseradish , mustard, and wasabi.  The bioactivating agent is an enzyme that is heavily modified after it has been synthesized in the plant.  We are investigating how these unusual post-translational modifications contribute to plant fitness in plant-herbivore interactions. 

Plants of the Solanum genus produce steroidal glycoalkaloids as defense compounds against generalist herbivores.  These compounds are the bitter flavors we associate with unripe tomatoes and the jackets of red potato tubers.  The production of these compounds requires increased metabolic flux through the terpenoid biosynthetic pathway.  The enzyme squalene synthase is a critical enzyme of this pathway and in potato is encoded by an unusually large gene family.  We are looking at the individual members of the gene family to identify biochemical and molecular features that contribute to the biosynthesis of the steroidal defense compounds.

tokuhisa@vt.edu
302 Fralin Hall
(540) 231-0344

Area:  EEB
The tree of life provides a roadmap for understanding evolution and the history of life. The Uyeda lab uses this map to understand how biological processes give rise to the large-scale patterns of diversity we see in nature. We focus on establishing a better connection between microevolutionary processes and the models we use to understand trait evolution at the macroevolutionary scale. We use a combination of methods development, theoretical work and empirical studies to synthesize biological data across scales to obtain a better understanding of what causes long-term evolutionary change. By synthesizing data from microevolutionary, paleontological and phylogenetic comparative studies into a cohesive framework, we can gain important insights into understanding when and why adaptation succeeds or fails over long evolutionary time-scales. This is especially important today as rapid global change is driving rapid evolutionary change. We must understand how these processes scale up over time if we wish biodiversity to persist for generations millennia to come.

juyeda@vt.edu
4076 Derring Hall
(540) 231-2119

Area: EEB, MCDCB
The Vargas-Muñiz Lab is interested in understanding the fundamental principles of fungal cell biology that impact fungal cell division, pathogenesis, and host-pathogen interactions. Our research program focuses primarily on how the cytoskeleton contributes to cell shape, emphasizing the septin cytoskeleton and the involvement of fungal septins in cell wall integrity. The fungal cell wall is a key structure that provides the mechanical force needed for fungi to survive in different environments, enables host tissue invasion, and facilitates the differentiation of different cell types. Moreover, the fungal cell wall is the first point of contact between the fungal pathogen and its host. Since mammalian cells lack a cell wall and plant cell walls are fundamentally different in composition and organization, the fungal cell wall has been an attractive target for antifungal development in the past, and understanding how fungi regulate their cell wall is key for combating fungal infections. Additionally, our research program aims to determine the cellular and molecular mechanisms behind how fungal morphologies change in reaction to stress utilizing marine fungi as our experimental model system.​

jvm15@vt.edu
383 Steger Hall
(540) 231-7421

svoshell@vt.edu
459 USLB
(540) 231-7818

rawalker@vt.edu
2097 Derring Hall
(540) 231-3803

Area:  EEB
Evolution of cooperative breeding in birds; ecological basis of sensitivity to habitat fragmentation; evolution of social behavior and life history in birds and primates; dispersal behavior; conservation of endangered birds

jrwalt@vt.edu
2104 Derring Hall
(540) 231-3847

Area:  EEB
Plant evolutionary responses to multi-species interactions;
chemical ecology of seed dispersal and fruit defense;
domestication and plant defense; agricultural applications of chemical ecology

swhitehead@vt.edu
408 Latham Hall
(540) 231-2137

bdwills@vt.edu
2082-D Derring Hall
(540) 231-9822

Area: MCDCB
Characterization of the architecture and localization of the Arabidopsis flavonoid enzyme complex using a variety of molecular, biochemical, and cell biological techniques; analysis of the effects of phytohormones on the plant root proteome and metabolome using mass spectrometry-based methods, in collaboration with the Helm Laboratory in the Department of Biochemistry and colleagues at Wake Forest University; development of novel multimetallic complexes for use as anticancer agents, in collaboration with the Brewer Laboratory in the Department of Chemistry.

winkel@vt.edu
2104 Derring Hall
(540) 231-3847

Area: Micro/Immuno
The bacterial type IV pilus (T4P) is a virulence factor in Neisseria gonorrheae, Pseudomonas aeruginosa, Acinetobacter baumannii, and Clostridioides difficile which are all identified by WHO and CDC as priority pathogens because of their prevalent and rising antimicrobial resistance (AMR). The ability of bacteria to form biofilms in and out of a human host is intimately intertwined with AMR and its environmental persistence and transmission. The major focus of the Yang lab is on the bacterial T4P with two main lines of investigation. One is to explore T4P as an antivirulence target against antibiotic-resistant bacterial pathogens. The other is to understand the role of T4P in regulating and mediating bacterial biofilm formation. Our research work involves Gram-negative bacteria and their phages as experimental materials. We have expertise in molecular biology, biochemistry, genetics and discovery of anti-T4P compounds as drug leads. We collaborate with scientists at Virginia Tech and elsewhere who have complementary expertise in medicinal chemistry as well as structural and computational biology.

zmyang@vt.edu
500 Derring Hall
(540) 231-1350