Alumni

Stephanie graduated from the University of Puerto Rico in Humacao (UPRH) in Fall 2020 with a B.S. in Microbiology. While at UPRH, she worked with Dr. Ezio Fasoli exploring microbial redox reactions as a tool for understanding metabolic systems. Stephanie is currently pursuing her PhD in the Microbiology and Molecular Genetics (MMG) Program at Emory University under the mentorship of Dr. Christopher LaRock. Stephanie’s thesis work focuses on understanding host-pathogen interactions during invasive S. pyogenes skin infections. The main aim of her project is to examine how host inflammation dictates S. pyogenes toxin production. The long-term goal of this work is to identify novel targets that stall disease progression, reducing high instances of morbidity and mortality associated with invasive S. pyogenes infections.

Pathogens must successfully prevent restriction by our formidable immune defenses in order to infect. This is often promoted by virulence factors specifically adapted to intercept key immune regulators. The LaRock laboratory examines how microbial virulence factors (eg. toxins and effectors) and host factors (eg. cytokines) interact, using biochemical, genetic, and pharmacologic tools. Our work is revealing new mechanisms of microbial pathogenesis, infection risks associated with immunotherapy, and new drug targets for infectious and autoinflammatory diseases. A long-term goal is to devise rational treatment strategies that enable effective immune clearance of an infecting pathogen without the dysbiosis or evolution of resistance that occurs with conventional antibiotics.



Pooja is a graduate student in the Molecular and Systems Pharmacology Program in the laboratory of Dr. Christine M. Dunham. She earned her B.A. Molecular & Cell Biology, University of California, Berkeley.

Christine M. Dunham, PhD, is a Professor of Chemistry, Emory College of Arts and Sciences. She earned her B.A. in Biochemistry at Barnard College, Columbia University. Dr. Dunham earned her Ph.D. in the Department of Chemistry and Biochemistry, University of California, Santa Cruz, Laboratory of Prof. William G. Scott, with the thesis entitled, "Structure and Function of an RNA enzyme".

Dr. Dunham was an American Cancer Society Postdoctoral Fellow, MRC Laboratory of Molecular Biology, Cambridge, England, in the Laboratory of Dr. Venki Ramakrishnan.

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Bill Wuest, PhD, is a Georgia Research Alliance Distinguished Investigator, a Professor in the Department of Chemistry in the Emory College of Arts and Sciences, and a member of the Emory Department of Chemistry Graduate Program. His research focuses on leveraging natural product total synthesis to better understand antibiotic mechanisms of action. His group utilizes synthetic chemistry, microbiology, genetics, and proteomic methods to develop novel compounds to combat bacteria. He earned his B.S. in Chemistry/Business at the University of Notre Dame, his Ph.D. in organic chemistry from the University of Pennsylvania, under the advisement of Prof. Amos B. Smith, III and was an NIH Postdoctoral Fellow in the lab of Prof. Christopher T. Walsh at Harvard Medical School.

Dr. Wuest is the recipient of a number of awards recognizing his research & scholarship including an NSF CAREER Award, the 2017 ACS Infectious Diseases Young Investigator Award, the 2020 David W. Robertson Award from the ACS Division of Medicinal Chemistry, the New Investigator Award from the Charles E. Kaufman Foundation, the Thieme Journal of Chemistry Award, the Young Investigator Award from the Center for Biofilm Engineering at Montana State University, and the Italia-Eire Foundation Distinguished Teacher of the Year Award from the College of Science and Technology at Temple University. He is also a 2019 AAAS Leshner Fellow and an RCSA Scialog Fellow. His research is currently supported by an NIH R35 MIRA grant and NSF funding.

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Ribosomal RNA (rRNA) modification is important for correct ribosome assembly, can alter ribosome function, and can confer resistance to many clinically important ribosome-targeting antibiotics in pathogenic bacteria. Unlike other ribosome-targeting antibiotics, such as macrolides and aminoglycosides, whose activity is blocked by methylation of the ribosome, the tuberactinomycn antibiotic capreomycin requires methylation at position C1409 of the 16S rRNA within the small ribosome subunit (30S) and C1920 of the 23S rRNA within the large ribosome subunit (50S). TlyA is the 2’-O-methyltransferase that modifies the ribose 2’- OH of C1409 and C1920 using S-adenosyl-methionine (SAM) as a methyl group donor. The X-ray crystal structure of the C-terminal domain (CTD) of TlyA showed that the domain adopts a Class I methyltransferase fold while homology modeling suggests the N-terminal domain (NTD) adopts an S4 ribosomal protein fold. Additionally, the structural studies of the CTD revealed that the short interdomain linker was able to adopt two different conformations and was unexpectedly critical for SAM binding within the CTD. These observations lead to a proposal that the interdomain linker might be able to act a “molecular switch” by altering the interaction between the NTD and the CTD and controlling TlyA activity upon correct substrate recognition. However, TlyA’s mechanism of recognition and modification of its target sites located in structurally distinct contexts is currently not known. In this project, he will test the hypothesis that TlyA is structurally and functionally divided: the NTD directs specific ribosome subunit recognition, the CTD performs catalysis of methylation, and the flexible linker controls essential communication between these two domains. The goal is to determine the mechanism of TlyA 30S/50S recognition and site-specific methylation of two distinct target nucleotides. He will accomplish this through the following two Specific Aims. The first aim is to define TlyA NTD surfaces and critical residues for recognition of the distinct 30S and 50S ribosomal subunit binding sites using site-directed mutagenesis followed by binding and methyltransferase assays. In my second aim, he will determine the molecular mechanism by which TlyA recognizes then methylates its target sites on the ribosome using studies of protein dynamics using hydrogen-deuterium exchange coupled to mass spectrometry, and high- resolution structures using X-ray crystallography and cryo-EM. This project will increase our understanding of not only TlyA’s mechanism of binding and modification but also those of other ribosome-modifying enzymes, expanding our limited understanding of how RNA modification enzymes control substrate specificity. 

Graeme L. Conn, PhD, is a Professor in the Department of Biochemistry, Emory University School of Medicine. His lab uses modern biochemical and biophysical methods to study the structures, interactions and biological functions of biomedically important RNA and protein molecules. Current topics include mechanisms of bacterial antibiotic resistance that arise through ribosomal RNA modification and non-coding RNA-mediated pathogen evasion of host cell innate immune responses.

Dr. Conn received his BSc and PhD at the University of Edinburgh, UK, and followed this with postdoctoral research as a Wellcome Trust International Fellow at the Johns Hopkins University, Baltimore, MD. Graeme was a faculty member at UMIST/ The University of Manchester, UK, from 2000 and joined the Department of Biochemistry at Emory as an Associate Professor in September 2008.

Samantha Prezioso received her BS in microbiology from the University of Maryland in 2010. During that time she did a yearlong internship with the FDA’s Center for Food Safety and Applied Nutrition in which she improved detection methods for paralytic shellfish poisons in clams, and later E. coli O157:H7 in leafy greens.  After graduation, she spent two years at the Centers for Disease Control and Prevention (CDC) in Atlanta, GA in the Department of Foodborne, Waterborne, and Environmental Diseases. There she worked on several projects with the goal of advancing bioterrorism preparedness through improved detection assays. One such project included a study of mutations in Bacillus anthracis conferring resistance to ciprofloxacin. Currently she is studying at Emory University in the lab of Dr. Joanna Goldberg, where she is investigating the regulation and cellular impact of EF-Tu trimethylation in Pseudomonas aeruginosa. Of particular interest is the emerging field of literature suggesting that modulation of cellular translation leads to persister cell formation; persister cells being those that survive antibiotic treatment without an acquisition of a resistance mechanism. She hopes to advance our understanding of this phenomenon through the completion of her graduate study, and proceed to a career investigating persisters and other timely topics in microbiology. 

Joanna B. Goldberg, PhD, is a Professor in the Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis and Sleep in the Department of Pediatrics at Emory University School of Medicine. She holds a secondary appointment in the Department of Microbiology and Immunology. Her research program focuses on bacterial genetics, genomics, and pathogenesis, with a particular emphasis on respiratory infections in cystic fibrosis, with the goal of developing novel therapies to prevent and treat chronic diseases.

Thayer received her Bachelor of Science degree in Biology from the University of Georgia in 2011. During her undergraduate research career she studied the protozoan parasite Toxoplasma gondii and worked on understanding molecular mechanisms essential for parasite survival. She continued this research after graduation before entering the Immunology and Molecular Pathogenesis program at Emory University in 2013. In continuation of her interest in parasite pathogenesis and host-pathogen interactions, she joined the lab of Dr. Tracey Lamb to study the immunopathogenesis of malaria, a disease caused by infection with protozoan parasites of the genus Plasmodium. The Lamb Lab is particularly interested in understanding the immune response during Plasmodium infection and how it contributes to disease pathogenesis as well as developing novel vaccination and therapeutic targeting strategies against Plasmodium infection. Thayer’s project focuses on understanding the role of Eph receptors in the immune response during cerebral malaria and exploring targeted therapeutic approaches against Eph receptors to prevent the development of disease. Malaria remains a severe global public health issue and the Antimicrobial Resistance and Therapeutic Discovery Training Program will allow her to expand her research to address the need for new adjunct therapies for malaria. 

Kara Phipps graduated in 2014 with a BS in Biology from Southwest Baptist University. While at SBU, Kara developed a strong interest in the study and control of infectious diseases and participated in undergraduate research.  Her studies focused on the relationship between DNA damage responses to fluoroquinolone treatment and biofilm formation and motility in Pseudomonas aeruginosa. Upon entering the Microbiology and Molecular Genetics program at Emory University, Kara joined the laboratory of Anice Lowen to study the factors which impact gene reassortment and diversification of influenza viruses. Kara particularly seeks to identify mechanisms which impact reassortment and viral diversification following transfer of influenza viruses to a non-native host species. With the opportunities and support provided by the Antimicrobial Resistance and Therapeutic Discovery Training Program, Kara hopes to further current knowledge of the basic mechanisms by which influenza viruses evolve to allow escape of current antiviral treatments and vaccine-induced immunity.

Anice C. Lowen, PhD, is Professor in the Department of Microbiology and Immunology, Emory University School of Medicine. She obtained her PhD from the University of Glasgow, UK, and carried out postdoctoral training at Mount Sinai School of Medicine in New York, NY.

Despite its clear importance to the epidemiology of influenza, the process by which human influenza viruses travel from one individual to another is not well understood. Prior to the zoonotic outbreak of H5N1 influenza viruses in Southeast Asia, it was generally assumed that if an influenza virus could productively infect a given host species, that virus would also transmit among individuals of that species. The lack of transmission of H5N1 influenza viruses among humans and other mammals has shown that, on the contrary, viral growth is not the only prerequisite for transmission. Research over the past six years has revealed that viral, host and environmental factors each play a role in determining the efficiency with which an influenza virus transmits. We previously showed, for example, that ambient conditions of humidity and temperature have a strong impact on the efficiency of transmission, that host-specific adaptive changes in the viral polymerase can alter transmission efficiency, and that host immunity resulting from either vaccination or natural infection limits transmission to varying degrees. Despite such progress, an in-depth understanding of transmission remains a high priority in the influenza field. Going forward, my research will focus on the viral traits which allow transmission to proceed in guinea pigs, a mammalian model system which we have demonstrated to reflect humans well in terms of influenza virus transmissibility.

Katie received her B.S. in Microbiology from Michigan State University in 2011. During her undergraduate study she worked with Neisseria gonorrhoeae investigating the impact of antimicrobials on the frequency of genetic competence. In continuation of her interest in antimicrobials, she is currently studying the impact of nutrition on the process of sporulation in Clostridium difficile in the McBride lab at Emory University. The CDC has currently ranked C. difficile as a major antibiotic resistance threat due to its natural capacity for resistance to a wide variety of antimicrobials.  A portion of these resistances are conferred by the spore form of C. difficile. The formation of the spore allows C. difficile to survive in the environment outside of the host and persist, especially in hospital environments. Spores are a metabolically dormant and are resistant to many antibiotics and disinfectants. The McBride lab works to understand the process of sporulation in hopes of discovering ways to limit sporulation and transmission of this antibiotic mediated disease. The Antimicrobial Resistance and Therapeutic Discovery Training Program will allow her to have the opportunity to take her research to conferences, both local and abroad. The issue of antimicrobial resistance is a global problem and at these conferences she will gain an international perspective of the issue and how others approach the problem of antimicrobial resistance.  Additionally, this program will allow her to take part in a variety of experiences that will familiarize her with how the issue of antimicrobial resistance is approached in industry, academia, and the clinic. 

Shonna M. McBride, PhD, is an Associate Professor in the Department of Microbiology and Immunology, Emory University School of Medicine. Research in the McBride laboratory centers on the emerging pathogen, Clostridium difficile. C. difficile is an spore-forming and toxin-producing bacterium that causes chronic intestinal disease which is both difficult and costly to treat. The two main factors that contribute to C. difficile infections are the ability of the bacterium to form resilient spores that allow the pathogen to spread, and the inherent resistance of the bacterium to antimicrobials. Current research topics in the lab include characterizing the genetic pathways that control spore formation, identifying mechanisms of resistance to antimicrobials, and investigating therapeutics to combat C. difficile infections. Research by the McBride lab has identified novel mechanisms used by this bacterium to respond to antimicrobial peptides, such as the CprABC transporter and the ClnRAB regulatory system, and a regulator of both toxin production and sporulation, RstA

Dr. McBride joined the Emory faculty in June 2012.  She received her Ph.D. degree from the University of Texas Health Science Center at San Antonio in 2005 and a Bachelor of Science degree from McNeese State University in 1999.  She trained as a postdoctoral fellow in the field of bacterial pathogenesis at the Schepens Eye Research Institute of Harvard Medical School from 2005 to 2008 and at the Tufts University School of Medicine from 2008 to 2012.  Dr. McBride’s research is supported by a K01 Career Development Award and an R03 Research grant from the NIDDK/NIH.  

Acinetobacter baumannii is a multidrug-resistant (MDR), Gram-negative nosocomial pathogen that exhibits two forms, distinguished by their opaque (O) and translucent (T) colony phenotypes.  The two variants have different patterns of gene expression, and notably, only the O variant is capable of infection.  Additionally, the O variant exhibits significantly greater resistance to host antimicrobial peptides, reactive oxygen species, hospital disinfectants, and to certain antibiotics including colistin.  The enhanced resistances of the O variant are especially worrisome as the MDR nature of A. baumannii already poses a considerable problem in treating infections, and colistin is often reserved as the last line option for treatment.  Colonies of the O and T variants rapidly interconvert, and therefore our group has focused on identifying and characterizing genes involved in this switch. My thesis objective is to thoroughly characterize ABUW_1132, a gene I recently discovered where loss of function mutations reduce O to T switching by 35-fold.  ABUW_1132 is predicted to encode a LysR-family transcriptional regulator, and preliminary data indicates it to be a major component of the O to T switch. This work will provide a more complete picture of the regulation of A. baumannii’s phenotypic switch, which is crucial to understanding infection by this pathogen and thereby formulating new methods of treatment.

Sarah Anderson received her BS in 2013 from the University of North Carolina, where she double majored in biology and chemistry.  As an undergraduate, Sarah conducted research projects on gene regulation in Drosophila melanogaster, and on innate immune responses to influenza infection.  Following graduation, she was awarded an APHL/CDC Emerging Infectious Diseases (EID) Fellowship to conduct research at the Wadsworth Center in the New York State Department of Health.  There she developed a diagnostic assay to detect fluoroquinolone-resistant Mycobacterium tuberculosis, and worked on a basic research project studying conjugation in Mycobacterium smegmatis.  Sarah enrolled in the Microbiology and Molecular Genetics program at Emory University in 2014.  Her interests in antibiotic resistance, bacterial genetics, and pathogenesis led her to join the laboratory of Dr. Philip Rather.  Sarah’s current research in the Rather lab focuses on understanding the mechanisms regulating phase variation and intrinsic antimicrobial resistance in Acinetobacter baumannii.  By participating in the Antimicrobial Resistance and Therapeutic Discovery Training program, Sarah hopes to expand her training outside of the laboratory by presenting her work at conferences and networking with scientists both inside and outside academia. 

Philip N. Rather, PhD, is a Professor in Microbiology and Immunology, Emory University School of Medicine. His lab studies the mechanisms of virulence and intrinsic antibiotic resistance in the nosocomial pathogen Acinetobacter baumannii. Dr. Rather's lab is studying cell-to-cell signaling in the human pathogen Acinetobacter baumannii with the goal of understanding the role of this process in virulence. These studies involve: (i) purification and structural characterization of extracellular signaling molecules, (ii) identification of genes involved in signal response, (iii) identification of genes involved in signal production, and (iv) the use of RNA-Seq to identify genes activated/repressed by extracellular signals.

A second area of study addresses the mechanisms that allow the urinary tract pathogen Proteus mirabilis to differentiate to swarmer cells. The role of a regulatory molecule, phenethylamine, in controlling the activity of a key transcriptional regulator (FlhDC) is being investigated.  In addition the Rather Lab is investigating the mechanisms that allow P. mirabilis to sense surfaces and transmit these signals to the regulation of gene expression.

I am interested in how the Gram-positive pathogen Staphylococcus aureus develops intermediate resistance to vancomycin; these strains are called VISA. My project tests the hypothesis that different VISA mutations have different fitness in two clinically important genetic backgrounds and are compensated by different mutations. Aim 1. Interaction of genetic background, mutation and fitness costs for vancomycin resistance level. I will determine how single nucleotide polymorphisms (SNPs) in candidate genes modulate vancomycin resistance to characterize mutations found in VISA strains by using isogenic USA100 and USA300 mutants and testing for a phenotypic effect on vancomycin resistance. Validated VISA determinants will be introduced into USA100 and USA300 MRSA lineages to investigate how vancomycin resistance alters the fitness and virulence of strains and ultimately the fitness landscape between lineages. Aim 2. Parallel evolution of vancomycin resistance and subsequent divergence. I will determine the convergent mutation in candidate genes of USA100 and USA300 by generating and sequencing laboratory VISA strains at different bottlenecking pressures. Maintenance of these VISA strains at sub-MIC antibiotic concentrations will allow for the study of divergence in evolution that will occur after selection pressures have decreased and more evolutionary pathways have opened. Together, these two approaches will be a comprehensive study of the evolution of vancomycin intermediate resistance in S. aureus and its effects on the fitness landscape.

Timothy D. Read, PhD, is a Professor of Infectious Diseases with a secondary appointment in Human Genetics, Emory University School of Medicine. Dr. Read's research interests center around the application of genomics technologies to understanding infectious diseases. In particular, he is interested in trying to frame the questions that only become possible to answer as new and even better instruments for generating DNA sequence information come online. Genomics for infectious disease detection and clinical diagnosis. The rapidly decreasing cost of sequencing offers the opportunity in the near future to rapidly acquire large portions of the genome sequence of pathogens, either from DNA extracted from pure cultures or directly from clinical samples (metagenomics).

Jessica Trost received her BS in Biology from the University of Wisconsin-Madison in 2007.  After graduation, she pursued work in pediatric respiratory virus research and clinical diagnostic development at the Medical College of Wisconsin.  Following the 2009 influenza pandemic, and inspired by the importance of preparedness, she applied and was awarded the APHL/CDC Emerging Infectious Disease (EID) fellowship at CDC and joined the Influenza Division.  At CDC, her work included detecting and evaluating potentially broadly neutralizing antibodies in influenza, vaccine strain selection, and the first evidence of influenza infection in sea otters.  Her current research at Emory University as a student in the Microbiology and Molecular Genetics (MMG) program in Dr. David Steinhauer’s lab focuses on understanding the relationship and balance of the two major surface glycoproteins of influenza, HA and NA.  Her aim is to understand the impact of these two proteins in the reassortment and emergence of novel and pandemic influenza viruses from natural avian reservoirs.  With the support of the Antimicrobial Resistance and Therapeutic Discovery Training Program, she hopes to evaluate the potential for novel influenza subtypes to emerge in naive human populations, or reassort with current influenza strains in humans, to highlight and improve vaccine and antiviral targets in advance of emerging epidemics and pandemics.  

David A. Steinhauer, PhD, is an Associate Professor of Microbiology and Immunology, Emory University School of Medicine. The Steinhauer laboratory is primarily interested in influenza virus entry into host cells and the role of the hemagglutinin glycoprotein (HA) in this process. The work has a strong focus on the structure-function relationships of HA with regard to its receptor binding and membrane fusion properties. The work combines protein structure analysis and molecular virology techniques to address specific questions on how influenza viruses attach to cells, deliver their genomes, assemble at the end of the replication cycle, and evolve to evade host immune responses and the action of antiviral drugs. We are also attempting to exploit our knowledge of high resolution HA structures to design novel vaccines for influenza, and for other pathogens using influenza as a vector.

Edgar Sherman received his BS from The University of Texas at San Antonio (UTSA) in 2014. Edgar developed a strong interest in microbial genetics following two research internships where he investigated the role of mitochondrial gene function in eukaryotic respiration at The University of Texas at Austin and studied how protein turnover affects aging in rodents at The University of Texas Health Science Center in San Antonio.  At UTSA, Edgar’s research focused on mechanisms of biofilm formation in the nosocomial pathogen Acinetobacter baumannii by targeting genes involved in bacterial cell signaling. After graduating, Edgar was accepted into the Microbiology and Molecular Genetics (MMG) program at Emory University where his research interest in antimicrobial resistance led him to join Dr. David Weiss’ lab and focus on studying antibiotic resistance mechanisms in Multi-drug resistant Gram-Negative pathogens. Specifically, Edgar’s research focuses on understanding the underlying genetic pathways facilitating resistance to aminoglycosides, an important class of antibiotics, in A. baumannii and how these mechanisms lead to treatment failure in a patient. Under the Antimicrobial Resistance and Therapeutic Discovery Training Program, Edgar seeks to characterize novel resistance mechanisms to ultimately improve patient outcome and expand our understanding on how bacteria evolve to combat our clinical therapeutics. 

Emily Crispell received her BS in Chemistry from the Georgia Institute of Technology in 2009. After graduation, she switched fields to pursue an interest in microbiology, infectious diseases, and epidemiology through a four-year position with the Georgia Emerging Infections Program (GAEIP) laboratory in Atlanta, GA. Her research with the GAEIP focused primarily on antibiotic resistance trends and mechanisms in Staphylococcus aureus. Her current research at Emory University in the laboratory of Dr. David Weiss focuses on novel antibiotic resistance mechanisms in multi-drug resistant Gram-negative pathogens and the development of inhibitors to target these resistance mechanisms. Particular research interests include how bacterial signaling systems govern the regulation of antibiotic resistance and how host factors influence the development of antibiotic resistance during bacterial infection. As a trainee of the Antimicrobial Resistance and Therapeutic Discovery Training Program, she aims to develop unique insight into the problem of antibiotic resistance by connecting basic science research training with mentorship from leaders in the clinic. 

David S. Weiss, PhD, is a Professor in the Division of Infectious Diseases, Emory University School of Medicine, and Co-Director of the Emory Antibiotic Resistance Center. His lab's research is focused on understanding mechanisms of antibiotic resistance employed by Gram-negative nosocomial pathogens such as Acinetobacter baumannii and Enterobacter cloacae. His lab has identified and mechanistically characterized several novel genes that contribute to resistance to the last-line, cationic polymyxin antibiotics in diverse bacteria. Furthermore, this research has shown that the development of polymyxin resistance in treated patients leads to cross-resistance to cationic antimicrobial peptides of the host innate immune system. Thus, polymyxin treatment may select for bacterial strains with increased virulence. In addition to how antibiotics may alter bacterial susceptibility to the immune system, his lab is very interested in exploring the causes of unexplained treatment failures in which antibiotic therapy is ineffective despite bacterial strains appearing to be susceptible to a given antibiotic.

Rachel received a B.S. in Ecology and Evolutionary Biology from Yale University and is currently a Ph.D. candidate in the Microbiology and Molecular Genetics program in the laboratory of Dr. Joanna Goldberg. She is studying how the opportunistic pathogen Pseudomonas aeruginosa senses and responds to temperature changes as it transitions from living in the environment to infecting a human. As temperature is an important stimulus for regulating virulence, a better understanding of thermoregulation in P. aeruginosa could inform the development of therapeutics to prevent and treat P. aeruginosa infections. 

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Joanna B. Goldberg, PhD, is a Professor in the Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis and Sleep in the Department of Pediatrics, Emory University School of Medicine. Dr. Goldberg holds a secondary appointment in the Department of Microbiology and Immunology, Emory University School of Medicine. Her research program focuses on bacterial genetics, genomics, and pathogenesis, with a particular emphasis on respiratory infections in cystic fibrosis, with the goal of developing novel therapies to prevent and treat chronic diseases.

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Cheyenne Lee graduated with a BS in biotechnology from The University of North Carolina at Pembroke in May 2019. At UNCP, she worked with Dr. Conner Sandefur on characterizing the antimicrobial properties of Lumbee Tribe herbal teas under the NSF-COMPASS and NIH-RISE programs. Currently, she is a Ph. D. candidate in the Microbiology and Molecular Genetics (MMG) program and an ARTDTP fellow at Emory University. Under the mentorship of Dr. Shonna McBride, Cheyenne’s project focuses on characterizing Clostridioides difficile sporulation initiation specifically through the activities of the KipI and KipA proteins and the histidine-kinase CD1579. Without the ability to form spores, C. difficile cannot be transmitted as efficiently through the environment to infect new hosts. Knowing this, Cheyenne’s project focuses on understanding how C. difficile forms the spores that make it easily transmissible so that new targets for novel therapeutics to inhibit sporulation initiation may be uncovered.

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Shonna M. McBride, PhD, is an Associate Professor in the Department of Microbiology and Immunology, Emory University School of Medicine. Research in the McBride laboratory centers on the emerging pathogen, Clostridium difficile. C. difficile is an spore-forming and toxin-producing bacterium that causes chronic intestinal disease which is both difficult and costly to treat. The two main factors that contribute to C. difficile infections are the ability of the bacterium to form resilient spores that allow the pathogen to spread, and the inherent resistance of the bacterium to antimicrobials. Current research topics in the lab include characterizing the genetic pathways that control spore formation, identifying mechanisms of resistance to antimicrobials, and investigating therapeutics to combat C. difficile infections. Research by the McBride lab has identified novel mechanisms used by this bacterium to respond to antimicrobial peptides, such as the CprABC transporter and the ClnRAB regulatory system, and a regulator of both toxin production and sporulation, RstA

Dr. McBride joined the Emory faculty in June 2012. She received her Ph.D. degree from the University of Texas Health Science Center at San Antonio in 2005 and a Bachelor of Science degree from McNeese State University in 1999. She trained as a postdoctoral fellow in the field of bacterial pathogenesis at the Schepens Eye Research Institute of Harvard Medical School from 2005 to 2008 and at the Tufts University School of Medicine from 2008 to 2012. Dr. McBride’s research is supported by a K01 Career Development Award and an R03 Research grant from the NIDDK/NIH.

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Hannah Smith earned her BS in Microbiology and Genomics & Molecular Genetics at Michigan State University and conducted undergraduate research under the mentorship of Dr. Christopher Waters. There, she used complementary genetic and biochemical approaches to investigate the interaction between the master biofilm regulator of Vibrio cholerae, VpsR, and the second messenger molecule cyclic-di-GMP to determine their contribution to biofilm formation. Hannah is currently a PhD candidate in the Microbiology and Molecular Genetics Program in the laboratory of Dr. Marcin Grabowicz where she is studying lipoprotein trafficking in Gram-negative bacteria like Escherichia coli.

Lipoprotein trafficking is essential for all Gram-negative bacteria, making this process an excellent target for novel antibiotics. In E. coli, the lipoprotein chaperone LolA traffics lipoproteins across the periplasm to the outer membrane lipoprotein receptor, LolB. Although the proteins involved in LolAB lipoprotein trafficking are known, their molecular mechanisms remain unknown; specifically, the way in which LolA binds lipoproteins is not known. Hannah is using several new genetic tools to uncover mechanisms of LolA function. Her projects will provide molecular-level details of lipoprotein trafficking across Gram-negative bacteria, which will enable design of novel antibiotics that target assembly of the outer membrane antibiotic barrier.

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Marcin Grabowicz, PhD, is an Associate Professor in the Department of Microbiology and Immunology with a joint appointment in the Department of Medicine, Division of Infectious Diseases, Emory University School of Medicine. Marcin completed postdoctoral training in the lab of Tom Silhavy at Princeton University, applying bacterial genetics to understand outer membrane biogenesis in Escherichia coli. The outer membrane is a highly selective permeability barrier that blocks antibiotics from entering Gram-negative bacteria. The Grabowicz lab is studying how the outer membrane is built and investigating strategies to disrupt this essential process.

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