I study insect-pathogen interactions, emphasizing questions such as how natural selection operates on host immune systems and why individuals vary in susceptibility or resistance to infection. I like to think of the host as an assemblage of interacting physiological processes where the immune system is embedded in the overall physiological context of the host. We consider host and pathogen as interacting components of a single system shaped by the abiotic environment.
The main focus of our research program is to elucidate key mechanistic components in enveloped viruses and their host cells that: 1) mediate viral entry into cells, 2) elicit cell immune responses, and 3) mediate viral egress from cells. These studies are leading to the development of diagnostic tools, new techniques, antiviral agents, and vaccines. Within the enveloped viruses, we focus a significant portion of our efforts on the deadly zoonotic Nipah and Hendra viruses.
Our research explores the impact of host behavior and nutritional needs on the evolution of intestinal symbionts. Current projects include the study of signals that coordinate the physiology and development of intestinal bacteria with the feeding activity of their host. We are also interested in the roles microbes play in providing nutritionally important organic molecules to herbivorous hosts.
The August lab is interested in infection-based and environment signals that trigger inflammation. We are particularly interested in signals regulated by the Tec family kinases, and how they regulate activation of cells such as mast cells and T cells to drive their differentiation and production of inflammatory cytokines.
The Blissard lab addresses fundamental questions on the biology and pathology of virus-insect interactions. A primary focus is the study of viral envelope glycoproteins and their interactions with host insect cells and cell proteins during viral entry and egress. Another focus are is understanding the gene expression program of the insect pathogenic virus, Autographa californica multiple nucleopolyhedrovirus (AcMNPV) and the transcriptional responses of the host insect cell.
Our research centers on crop diseases caused by Xanthomonas bacteria, focusing on TAL effectors injected by the bacteria to manipulate host gene expression after discovering how TAL effectors recognize their DNA targets and pioneered their use as tools for experimental gene regulation and genome editing. Current efforts focus using TAL effectors to generate plant disease resistance.
I study how microbes in the human microbiome are transmitted among individuals, using a wide range of approached including shotgun metagenomics of mircobiome communities, culture-based methods, and single-cell analyses. Another main focus is horizontal transmission of genes between members of the microbiome, specifically focusing on genes conferring antibiotic resistance.
The Buchon lab focuses on the impact of pathogens and the microbiota on body homeostasis. We use systemic infection as a model for septicemia, and the gut response to infection as a model for mucosal immunity. Genomic and genetic approaches allow us to characterize new pathways involved in both resistance and tolerance to infection. Specifically, we are interested in the three-way dialogue between gut microbes, intestinal stem cells, and gut structure and function.
My research program explores soil microbiome dynamics and their impacts on ecosystem health, the plants we grow, the water we drink, and the air we breath. We use genomic approaches to examine the ecological and evolutionary mechanisms that regulate microbial diversity and its impact on our world.
Numerous studies demonstrate that vector-borne pathogens influence host characteristics, resulting in altered host-vector interactions and enhanced transmission. We seek to determine the molecular mechanisms that underlie this phenomenon and use this knowledge to develop innovative control strategies using genetic and biochemical approaches. Current focuses are on changes in plant signaling and defenses, cell biology, and protein functions in response to insect vectors.
Our research seeks to understand how the host immune system is regulated by the gut microbiota through their secretion of small molecule metabolites. We focus primarily on two areas: 1) the identification of metabolites produced by the gut microbiota that regulate the host immune system, and, 2) the development of chemical tools to modulate the immune response.
My research focuses on the pathogenesis of bacterial diseases and vaccine protection mechanisms. My lab is working on the interaction of host receptors and virulence factors of C. difficile (toxins), Leptospira spp, and F. nucleatum (adhesins). We are also working on the mucosa immunity against F. nucleatum and M. avium subsp. paratuberculosis using outer membrane vesicle delivery systems, with the goal of developing a vaccine against human colon cancer and Johne’s disease.
We study the molecular evolution and population genetics of the immune system in Drosophila and other insects, specifically focusing on comparative genomics and transcriptional regulation of the immune response. We also explore host genetic variation in microbiome composition and function in a large human twin study and in the mouse model.
The Dhondt lab has studied the bacterial disease mycoplasmal conjunctivitis since it emerged in birds around 1994. We currently study effects of coinfection by combining studies of Mycoplasmal gallisepticum, haemosporidian parasites and other pathogens in the same individual. Students participate in both field work (trapping, handling, and sampling birds) and lab work, as well as study blood smears to detect the presence of haemosporidian parasites.
My group studies cell envelope stress responses of Gram-negative pathogens. We are defining regulatory pathways and functional networks of enzymes involved in cell wall degradation, modification and synthesis as well as factors required for upholding outer membrane barrier function. We seek to understand these processes to gain insight into the mechanistic underpinnings of cell growth and shape, as well as antibiotic resistance.
We investigate the interactions between animals and beneficial microbes as a biomedical model for human health and a novel target for insect pest control.
My research is focused on the eukaryotic cell DNA damage response (DDR) to a novel bacterial genotoxin called cytolethal distending toxin (CDT) within the context of intestinal disease of human and animals. I also have extensive experience in the development and assessment of laboratory animal models of disease and molecular mechanisms of host-pathogen interactions.
I am a theoretical ecologist working on disease transmission in multi-species communities characterized by functional traits. Students and postdocs in my research group have worked on a variety of projects related to control of invasive species in heterogeneous landscapes.
Parasite life history strategies within the host, especially the timing of replication and transmission, influence disease severity and spread. I study how subtle differences in ecology within and outside the host can generate dramatic differences in parasite strategies. My research program uses two major approaches: (1) building ecologically-detailed models to ask when and why particular strategies would be favored; and (2) developing novel statistical approaches to better characterize parasite traits from existing data.
Emphasis is on pathogens and symbionts of invertebrates, predominantly focusing on interactions between microbes and insect hosts, many of which are invasive species. Subjects covered are broad, ranging from population biology, immune responses, basic biologies of pathogens, interactions between hosts and pathogens and epizootiology to use microbes for control of insect pests.
My research focuses on the biology, ecology and behavior of mosquitoes that transmit human diseases such as dengue fever, West Nile virus and malaria. I have developed methods for studying blood feeding patterns, survival and longevity, mating behavior and feeding behavior of mosquitoes in both the laboratory and field. I am additionally interested in evaluating mating competition and fitness of transgenic mosquitoes prior to field deployment.
Most flowering plants develop mutualistic symbioses with arbuscular mycorrhizal (AM) fungi to improve access to essential mineral nutrients. The fungal endosymbionts are housed in membrane-bound compartments within root cells. Our research combines genetic, genomic and cell biology approaches to dissect the plant and fungal cellular programs for establishment and regulation of AM symbiosis, and mechanisms of symbiotic phosphate transport.
We study the transmission and impacts of infectious disease in a changing ocean and mechanisms of immune function in marine invertebrates. We work to identify the value of intact ocean biodiversity and develop strategies towards a healthier ocean.
Our research uses a combination of molecular, genetic, and proteomics approaches to understand how insects transmit plant pathogens and how pathogens manipulate host plants to ensure replication and transmission. A second are of research is the development of new pest management tools to enhance cultural control and to provide new management strategies for insect vector-borne diseases in plants.
We use Bacillus subtilis as a model system to characterize the bacterial stress responses elicited by metal ion limitation and excess during infection, and by host-produced antibiotics that interfere with integrity of the cell envelope. The resulting insights are relevant for understanding the mechanisms that allow bacterial cells (both beneficial and harmful) to adapt to the host environment.
While Hendry is broadly interested in the evolution and ecology of bacteria interacting with hosts, work in the Hendry lab aims to integrate data from genomic, experimental and field research to determine how host interactions shape bacterial evolution and population dynamics, and how these factors then impact hosts. We use a variety of systems to address these questions, particularly interactions of plant-associated bacteria with herbivorous insects.
Our research focuses on orthopaedic disorders and how they are regulated by physical forces and bacteria. Our work includes collaborations with Orthopaedic surgeons at the Hospital for Special Surgery, examination of the microbiome and orthopaedic disorders in mice and the role of physical forces in bacterial physiology and growth.
Our lab is interested in understanding mechanisms of lipid dependent host-microbe interactions and how these interactions influence human health. We use techniques in high-throughput sequencing, mass spectrometry based lipidomics, and general molecular biology to address these topics.
The goal of the Kao-Kniffin Lab is to understand the functional role of rhizosphere microbiomes in modifying plant traits. The rhizosphere harbors a tremendous diversity of soil microorganisms that enhance or inhibit plant growth. We are applying concepts in ecology and evolution to assemble microbiomes across generations that collectively modulate plant traits or ecosystem function.
Our research is focused on understanding how plants protect themselves against microbial pathogens at molecular and cellular levels. Major goals are to determine the mechanisms of salicylic acid (SA) activation and regulation of the plant’s immune responses, and to identify new targets or aspirin (acetyl SA) and its major metabolite SA in humans.
The Leifer lab investigates how the immune system detects and initiates inflammatory responses to microbes. Our focus is on regulatory mechanisms that control signaling through a class of innate immune receptors, Toll-like receptors.
The Martin lab studies the molecular bases of bacterial infection processes and the plant immune system. Our research focuses on speck disease caused by the bacterial pathogen Pseudomonas syringae pv. tomato. We use diverse experimental methods in biochemistry, bioinformatics, cell biology, forward and reverse genetics, genomics, molecular biology, plant pathology, and structural biology.
Our lab is focused on pollinator health. Specifically: 1) combining empirical data with network modeling to understand pathogen transmission in complex plant-pollinator networks, 2) evaluating the relative importance of pesticides, pathogens, and other factors on colony performance, and, 3) understanding how pesticide and pathogen stress influence bee behavior and delivery of pollination service to agriculturally important crops.
Research in my group focuses on the population genetics of rapid evolution, using a combination of experimental and modeling approaches. We are particularly interested in human-induced examples of rapid evolution, like the evolution of pesticide and drug resistance. We also study the possibility of population-scale genetic engineering by CRISPR-based gene drives, which promise powerful applications in the fight against vector-borne diseases, such as malaria.
We are studying the evolution of hots-microbe relationships. Our current work focuses on vertebrates’ co-evolutionary histories with microorganisms through a combination of -omics approaches, gnobiotic experiments, and field studies.
The Moreau lab focuses on the symbiotic factors that drive speciation, adaptation, and evolutionary diversification. Much of the research in the lab focuses on the potential co-evolution of ants and the gut-associated bacteria to understand the diversity and putative function of host-associated microbes. Combined with data on diet, trophic ecology, evolutionary history and biogeography, we hope to illuminate how these intimate interactions influence patterns of biological diversity.
A main driver of vector-borne disease transmission is the ecology of the insect vector. Changes in climate and land use alter ecological relationships insect vectors have with their hosts and pathogens, resulting in shifts in transmission. The research in the Murdock lab applies ecological and evolutionary theory to better understand the host-vector-pathogen interaction, key environmental drivers of transmission, and how environmental change will affect vector-borne disease transmission and control.
My research spans infection biology across scales and systems, utilizing a variety of theoretical and computational approaches, like: modeling of infectious disease dynamics in complex populations, networks and landscapes; characterizing the structure, function and evolution of cellular networks involved in microbial pathogenesis, and; probing the logic of information processing underlying recognition, communication, disruption and evasion in host-pathogen interactions.
We study disease resistance in maize and sorghum with a substantial focus on fungal pathogens that produce toxins and cause large-scale food system contamination. We work at scales ranging from a single nucleotide (which genetic variations provide quantitative resistance) to whole-plant phenotypes (looking at tradeoffs between resistance mechanisms and other traits) to agroecologies (what environmental factors lead to plant stresses associated with mycotoxin outbreaks).
The Parker lab uses the mammalian orthoreovirus model system and other human viruses to study virus-host interactions at the molecular and cellular level. Current projects are focused on the mechanisms viruses use to overcome translational repression and optimize translation of viral mRNAs, as well as mechanisms of feline calicivirus receptor interactions and entry.
My laboratory studies canine parvovirus, which is a cat virus that transferred into dogs in the 1970s to cause global pandemic of disease, and the H3N8 and H3N2 canine influenza viruses, which transferred from horses or ducks to dogs to cause two epidemics of canine disease that are still continuing. Our work seeks to examine the general basis of viral emergence, including risk factors associated with origins of new viruses in humans.
The Pawlowska lab studies the mechanisms underlying interactions between fungi and bacteria. We are interested in both, mutualisms and antagonisms. In mutualistic interactions, we want to discover novel mechanisms that stabilize these symbioses over evolutionary time. In antagonisms, we explore defense mechanisms that protect fungi from bacterial infections.
The central focus of the Peters lab is microbial evolution with mobile genetic elements. We are interested in how highly evolved mobile elements contribute to evolving new functions with a strong focus on emerging pathogens and antibiotic resistance. We use a combination of tools, but primarily bioinformatics, molecular genetics, and biochemistry.
We are interested in understanding the interactions between nutrition, host factors, and oral and gut microbiomes and the resulting effects on host physiology. This knowledge will help us determine how we can perturb the microbiome to alleviate and prevent metabolic disorders such as obesity and diabetes.
The Rudd lab is interested in how microbes alter immune development and how the adaptive immune system protects the host against acute and chronic pathogens.
My program is focused on drug discovery and the pathogenesis of infectious human disease. We work closely with the Gates Foundation and the California Institute for Biomedical Research to run high-throughput drug screening on Mycobacterium tuberculosis within the context of the host. We also have human subjects research programs in Malawi and South Africa that explore TB and HIV infections supported by the NIH and the Gates Foundation.
Dr. Schang uses small molecules with drug-like properties to probe the ways viruses cause infections. He is most interested in finding common features among the many viruses that cause disease in animals or humans, including how they enter cells and how they replicate and cause disease. He is also uncovering important information on how to use only a few drugs to fight infections with many different viruses, or even stop them before they start.
Our research is directed at characterizing structures and biological function of biogenic small molecules (BSMs) that regulate development and immune responses in plants and animals and serve important functions with associated microbiota. Using comparative metabolomic approaches we have engaged in a comprehensive effort to characterize structures and functions of all BSMs (more than 20,000 small molecules) produced by the model organism Caenorhabditis elegans, with a specific cofus on signaling molecules that regulate organismal development and interactions with microbiota.
My research group focuses on free-ranging North America wildlife to improve health outcomes across a variety of species, their pathogens and parasites. At the Cornell Wildlife Health Lab, we derive solutions from novel mathematical applications, innovative diagnostic evaluations, field-based studies, and human dimensions of wildlife diseases.
Two main areas of study in the Smart lab include identifying genes in bacterial pathogens that enable movement within a plant, and understanding the population diversity of rapidly reproducing oomycete pathogens. These studies enhance our knowledge of pathogen virulence determinants and further elucidate how plants recognize and respond to pathogens.
My laboratory studies Salmonella Typhi pathogenesis, with an emphasis on the action of typhoid toxin and the host response, and the development of potential prophylactics and therapeutics to aid in the prevention and treatment of typhoid fever. We also seek new bactericidal molecules to treat multidrug-resistant Salmonella spp. We take a multidisciplinary approach using genetic/genomic and proteomic methods, cell biology, immunology and biochemistry.
The Turgeon lab works on mechanisms of fungal virulence to plants with particular emphasis on the roles of fungal secondary metabolites, iron and oxidative stress. Classical genetic, molecular genetic, and genomic approaches are used.
We study how M.tuberculosis is capable of surviving within humans for decades in the face of a fully competent immune response. Our focus is primarily on the bacterial pathways, innate immunity, and the evolution of bacterial drug resistance in mammalian hosts.
My lab studies how stress and social interactions alter the biological state of organisms that experience them. Much of our work uses free-living passerine birds, including tree swallows, as model systems to test the neuroendocrine, epigenetic, and gut microbial impacts of stress and social connectedness, and their fitness effects.
My lab has a broad interest in the structure and function of viral envelope proteins, and how genomic mutations lead to changes in the envelope proteins and control viral pathogenesis. We primarily study influenza viruses of humans and animals, and coronaviruses, principally, SARS-CoV, MERS-CoV and feline coronaviruses. We are developing novel vaccines and diagnostic tests.
I am an ecosystem ecologist interested in the patterns, mechanisms, and consequences of the interactions between terrestrial ecosystems and the environment. My research program uses process-based ecosystem models as ‘numerical greenhouses’ to integrate the every-increasing heterogeneous data sets in ecology (e.g. synthesis in traits, ground census, flux tower, and remote sensing) and to conduct experiements that help to answer the above questions.
Most students and researchers in my lab work on questions related to amphibian diversification and conservation. Projects currently ongoing in the lab focus on disease resistance in amphibians, especially the spread and impact of the chytrid fungus Batrachochytrium dendrobatidis.