CIHMID Postdoctoral Fellows Program
The following is a list of potential projects in CIHMID host labs that prospective applicants to the CIHMID Postdoctoral Fellows Program could use as a basis for initiating contact with potential hosts.
Applicants are not required to choose a project from this list. Novel projects that are not on this list can be proposed, and applicants may apply to work with host labs who are not actively listing projects on this page.
This list will be continuously updated as new prospective projects arise.
Applicants are not required to choose a project from this list. Novel projects that are not on this list can be proposed, and applicants may apply to work with host labs who are not actively listing projects on this page.
This list will be continuously updated as new prospective projects arise.
Ilana Brito Lab: Horizontal Gene Transfer in the Human Microbiome
The Brito Lab uses systems-level approaches to assay function within the human microbiome. We are interested in postdocotral candidates proposing projects exploring interactions between the host and native microbiota at the molecular level and in those that address the fundamental ways in which the microbiome provides resiliency against infection or promotes vaccine efficacy. We are also focused quite heavily on the spread of antibiotic resistance determinants through the process of horizontal gene transfer. Experience working any of the following is preferred, but not required: anaerobic culture, mouse infection models, germ-free mice, cloning, next-gen sequencing, microbial genomics, or bioinformatics. Interested applicants should contact Ilana Brito (ibrito@cornell.edu) to discuss their proposals.
The Brito Lab uses systems-level approaches to assay function within the human microbiome. We are interested in postdocotral candidates proposing projects exploring interactions between the host and native microbiota at the molecular level and in those that address the fundamental ways in which the microbiome provides resiliency against infection or promotes vaccine efficacy. We are also focused quite heavily on the spread of antibiotic resistance determinants through the process of horizontal gene transfer. Experience working any of the following is preferred, but not required: anaerobic culture, mouse infection models, germ-free mice, cloning, next-gen sequencing, microbial genomics, or bioinformatics. Interested applicants should contact Ilana Brito (ibrito@cornell.edu) to discuss their proposals.
Stephen Ellner, Nicolas Buchon and Brian Lazzaro: Systems dynamics of stochastic infection outcomes in Drosophila
A central question in infection biology is to understand why two individuals exposed to the same pathogen may have life-versus-death differences in outcome. Host or pathogen heterogeneity is a natural explanation, but even when this is drastically constrained (genetically identical hosts reared together, identical infection protocols) we have found that many bacterial pathogens in Drosophila melanogaster have bimodal outcomes, with some hosts dying at high bacteria burden while others survive indefinitely with a persistent but fairly asymptomatic infection. We have previously constructed a conceptual model, based on experimental results, wherein pathogen proliferation rate and timing of host immune response interact to determine the outcome (Duneau et al, eLife 2017;6:e28298). We now seek a quantitative biologist to develop and test process-based system dynamics models to understand mechanistically when and how bimodal outcomes can be robust across a wide region of parameter space. Modeling should be complemented by theoretical and empirical study of host immune kinetics and bacterial behavior, to identify which processes govern the dynamics and outcome of the host-pathogen interaction.
A central question in infection biology is to understand why two individuals exposed to the same pathogen may have life-versus-death differences in outcome. Host or pathogen heterogeneity is a natural explanation, but even when this is drastically constrained (genetically identical hosts reared together, identical infection protocols) we have found that many bacterial pathogens in Drosophila melanogaster have bimodal outcomes, with some hosts dying at high bacteria burden while others survive indefinitely with a persistent but fairly asymptomatic infection. We have previously constructed a conceptual model, based on experimental results, wherein pathogen proliferation rate and timing of host immune response interact to determine the outcome (Duneau et al, eLife 2017;6:e28298). We now seek a quantitative biologist to develop and test process-based system dynamics models to understand mechanistically when and how bimodal outcomes can be robust across a wide region of parameter space. Modeling should be complemented by theoretical and empirical study of host immune kinetics and bacterial behavior, to identify which processes govern the dynamics and outcome of the host-pathogen interaction.
Tobias Doerr: Acinetobacter baumannii cell wall turnover, pathogenesis and antibiotic resistance
Acinetobacter baumannii is a notorious emerging pathogen that is often acquired in the hospital setting and readily develops resistance against multiple antibiotics. Its mechanisms of pathogenesis and growth regulation are poorly understood. This project aims at interrogating the cell biology, biochemistry and role in pathogenesis of cell wall turnover processes. Using genetic and proteomic screens as well as protein localization studies, we will establish the cell biology and biochemistry of cell wall turnover proteins (‘autolysins’, e.g. endopeptidases and lytic transglycosylases) and study their effect on growth and shape maintenance as well as susceptibility to antibiotics. Lastly, we will study autolysins’ contribution to A. baumannii pathogenesis using a mouse model of pneumonia, in collaboration with Jeongmin Song’s lab.
Acinetobacter baumannii is a notorious emerging pathogen that is often acquired in the hospital setting and readily develops resistance against multiple antibiotics. Its mechanisms of pathogenesis and growth regulation are poorly understood. This project aims at interrogating the cell biology, biochemistry and role in pathogenesis of cell wall turnover processes. Using genetic and proteomic screens as well as protein localization studies, we will establish the cell biology and biochemistry of cell wall turnover proteins (‘autolysins’, e.g. endopeptidases and lytic transglycosylases) and study their effect on growth and shape maintenance as well as susceptibility to antibiotics. Lastly, we will study autolysins’ contribution to A. baumannii pathogenesis using a mouse model of pneumonia, in collaboration with Jeongmin Song’s lab.
John Helmann Lab: B. subtilis responses to metal ion abundance and antibiotic stress
The innate immune system restricts the growth of invading bacteria by limiting access to essential nutrient metal ions (nutritional immunity) and by production of antimicrobial peptides and enzymes that attack the cell envelope. Using Bacillus subtilis as a model system, we characterize the bacterial stress responses elicited by metal ion limitation and excess, and by 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.
The innate immune system restricts the growth of invading bacteria by limiting access to essential nutrient metal ions (nutritional immunity) and by production of antimicrobial peptides and enzymes that attack the cell envelope. Using Bacillus subtilis as a model system, we characterize the bacterial stress responses elicited by metal ion limitation and excess, and by 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.
Tory Hendry Lab:
Host response to virulent bacterial pathogens
The Hendry lab studies interactions between epiphytic bacteria (Pseudomonas syringae) and agricultural pest insects. Many strains of bacteria commonly found on plants are also highly infective and virulent to insects such as aphids. The mechanisms and consequences of these interactions are poorly understood. Several opportunities for work on the system are available (contact Dr. Hendry for details), but of particular interest is the host response to infection. This project would categorize the progression of infection within hosts, as well as the host’s immune and/or non-immunological defenses.
Ecological genomics in a host-restricted luminous symbiont
Most luminous symbionts live in varied habitats and have large, diverse genomes. The luminous bacterial mutualists of flashlight fish, however, have undergone extreme genomic reduction (Hendry et al., 2016, Genome Biology and Evolution, 8:2203-2213). The genomes of these bacteria show signatures of adaptation to restricted habitats, including living as environmental cells in seawater and as closely host-associated symbionts. The goal of this project is to elucidate symbiont ecology through multiple approaches, including transcriptomics, laboratory assays, and functional metagenomics. Functional insights from this highly reduced system will
illuminate how bacteria adapt to their environment and hosts.
Host response to virulent bacterial pathogens
The Hendry lab studies interactions between epiphytic bacteria (Pseudomonas syringae) and agricultural pest insects. Many strains of bacteria commonly found on plants are also highly infective and virulent to insects such as aphids. The mechanisms and consequences of these interactions are poorly understood. Several opportunities for work on the system are available (contact Dr. Hendry for details), but of particular interest is the host response to infection. This project would categorize the progression of infection within hosts, as well as the host’s immune and/or non-immunological defenses.
Ecological genomics in a host-restricted luminous symbiont
Most luminous symbionts live in varied habitats and have large, diverse genomes. The luminous bacterial mutualists of flashlight fish, however, have undergone extreme genomic reduction (Hendry et al., 2016, Genome Biology and Evolution, 8:2203-2213). The genomes of these bacteria show signatures of adaptation to restricted habitats, including living as environmental cells in seawater and as closely host-associated symbionts. The goal of this project is to elucidate symbiont ecology through multiple approaches, including transcriptomics, laboratory assays, and functional metagenomics. Functional insights from this highly reduced system will
illuminate how bacteria adapt to their environment and hosts.
Teresa Pawlowska and Gillian Turgeon Labs: Understanding fungal innate immunity
The goal of this project is to elucidate mechanisms of innate immunity in early-diverging soil fungi Mucoromycotina. Unlike other filamentous fungi, Mucoromycotina encode few genes for secondary metabolite biosynthesis and do not synthesize extracellular antibacterial secondary metabolites that suppress antagonistic microbes. Instead, they appear to respond to bacterial antagonists by mounting a potent reactive oxygen burst and altering their cell wall composition, which prevents bacterial entry into fungal hyphae. The project is a collaboration between two SIPS scientists, a symbiosis expert Teresa Pawlowska and a fungal geneticist Gillian Turgeon. How antagonistic bacteria are recognized by the fungus and how this information is transduced to elicit its defensive responses are the two main questions to be addressed in the course of the project.
The goal of this project is to elucidate mechanisms of innate immunity in early-diverging soil fungi Mucoromycotina. Unlike other filamentous fungi, Mucoromycotina encode few genes for secondary metabolite biosynthesis and do not synthesize extracellular antibacterial secondary metabolites that suppress antagonistic microbes. Instead, they appear to respond to bacterial antagonists by mounting a potent reactive oxygen burst and altering their cell wall composition, which prevents bacterial entry into fungal hyphae. The project is a collaboration between two SIPS scientists, a symbiosis expert Teresa Pawlowska and a fungal geneticist Gillian Turgeon. How antagonistic bacteria are recognized by the fungus and how this information is transduced to elicit its defensive responses are the two main questions to be addressed in the course of the project.
Scott McArt Lab: Pollinator health: Disruption of pathogen blocking by fungicide-mediated alterations to bee microbiota?
Fungicides are the most commonly encountered pesticides by bees. We have recently found that fungicide exposure is the best predictor of gut pathogen (Nosema bombi) prevalence and range contractions in declining US bumble bees (McArt et al. 2017 Proc. Roy. Soc. Lond. B). Previous laboratory studies have found that fungicide exposure and Nosema infection can alter bee microbiota, yet whether these stresses are linked such that fungicides increase bee susceptibility to pathogens via microbiota alteration remains untested. With state-of-the-art analytical chemistry, molecular biology and bee rearing equipment and facilities, our lab is uniquely positioned to address these questions. Work in this area has the potential to unravel complex interactions between pesticides, microbes and bees, potentially leading to management recommendations that reduce stress on bees and improve pollinator health.
Fungicides are the most commonly encountered pesticides by bees. We have recently found that fungicide exposure is the best predictor of gut pathogen (Nosema bombi) prevalence and range contractions in declining US bumble bees (McArt et al. 2017 Proc. Roy. Soc. Lond. B). Previous laboratory studies have found that fungicide exposure and Nosema infection can alter bee microbiota, yet whether these stresses are linked such that fungicides increase bee susceptibility to pathogens via microbiota alteration remains untested. With state-of-the-art analytical chemistry, molecular biology and bee rearing equipment and facilities, our lab is uniquely positioned to address these questions. Work in this area has the potential to unravel complex interactions between pesticides, microbes and bees, potentially leading to management recommendations that reduce stress on bees and improve pollinator health.
