Background
Dr. Tamara O’Connor is an Assistant Professor of Biological Chemistry at the Johns Hopkins University School of Medicine and Director of Admission for the Graduate Program in Biological Chemistry. Dr. O’Connor’s research focuses on the molecular basis of infectious disease with a particular emphasis on the network of molecular interactions acting at the host-pathogen interface and pathogen evolution in natural reservoirs.
Dr. O’Connor received her Ph.D. in Biochemistry from McMaster University, Canada where she studied multicellular differentiation of the bacterium Streptomyces coelicolor with Dr. Justin Nodwell. She completed her postdoctoral training dissecting virulence mechanisms of the respiratory pathogen Legionella pneumophila with Dr. Ralph Isberg at Tufts University School of Medicine. She joined the Johns Hopkins faculty in 2013.
Dr. O’Connor is a member of the American Society for Microbiology and the American Society for Biochemistry and Molecular Biology. Dr. O’Connor received an Innovation Award from the Johns Hopkins University School of Medicine Discovery Fund, a Discovery Award from the Johns Hopkins University School of Medicine Fisher Center and was a Natalie V. Zucker Scholars Fellow and recipient of an Ontario Graduate Scholarship and a Bank of Montreal Graduate Scholarship in Science and Technology.
Centers and Institutes
Videos
Recent News Articles and Media Coverage
- Tamara O’Connor on Legionella bacteria using nature’s Trojan horse
- Tamara O’Connor on Legionella as a tool to discover new antibiotics
Research Interests
Microbial pathogenesis, pathogen evolution, antibiotics
Research Summary
The O’Connor lab studies bacterial pathogenesis focusing on defining the mechanisms by which bacterial pathogen establish infection, how they exploit host cell machinery to accomplish this, and how individual virulence proteins and their component pathways coordinately contribute to disease. In parallel, the O’Connor lab investigates how virulence strategies arise in environmental reservoirs as a consequence of bacterial interactions with protozoa and the role of these natural hosts in driving bacterial transmission and disease in humans. Using genetics, biochemistry, molecular and cellular biology, and functional genomics, the O’Connor lab examines the repertoires of virulence proteins required for growth in a broad assortment of hosts, how the network of molecular interactions differs between hosts, and the mechanisms by which bacterial pathogens cope with this variation.
O’Connor Lab – Lab website is currently under construction and will be available soon
Selected Publications
- O’Connor TJ, Boyd D, Dorer M, Isberg RR (2012) Aggravating genetic interactions allow a solution to redundancy in a bacterial pathogen. Science 338:1440-1444
- Boamah DK, Zhou G, Ensminger AW, O’Connor TJ (2017) From many hosts, one accidental pathogen: the diverse protozoan hosts of Legionella. Front Cell Infect Microbiol. 7:477
- Ghosh S and O’Connor TJ (2017) Beyond paralogs: the multiple layers of redundancy in bacterial pathogenesis. Front Cell Infect Microbiol. 7:467
- Park JM, Ghosh S, O’Connor TJ (2020) Combinatorial selection in environmental hosts drives the evolution of a human pathogen. Nat Microbiol. 5:599
- Boamah D, Gilmore MC, Bourget S, Ghosh A, Hossain MJ, Vogel JP, Cava F, O’Connor TJ, (2023) Peptidoglycan deacetylation controls Type IV secretion and the intracellular survival of the bacterial pathogen Legionella pneumophila. Proc Natl Acad Sci USA. 120:e2119658120.
- Ghosh S, Bandyopadhyay S, Smith DM, Adak S, Semenkovich CF, Nagy L, Wolfgang MJ, O’Connor TJ. (2023) Legionella usurps host cell lipids for vacuole expansion and bacterial growth. PLoS Pathogens. 20:e1011996.
- Shin CJ and O’Connor TJ. (2024) Novel induction of broad-spectrum antibiotics by the human pathogen Legionella. mSphere. e0012024.
Honors
- Fisher Center Discovery Program Award, Johns Hopkins University School of Medicine, 2018
- Discovery Fund Innovation Award, Johns Hopkins University School of Medicine, 2014
- Natalie V. Zucker Research Scholars Postdoctoral Fellow, 2009
- Graduate Research Fellow, Ontario Graduate Scholarship Fund, 2003
- Graduate Research Fellow, Bank of Montreal Graduate Scholarship in Science and Technology, 2002
- Graduate Program Affiliations
- Biological Chemistry (BC) Graduate Program
- Biochemistry, Cellular and Molecular Biology (BCMB) Graduate Program
- Immunology (IMM) Graduate Program
- Cellular and Molecular Medicine (CMM) Graduate Program
- Cross Disciplinary Graduate Program in Biomedical Sciences (XDBio)
Memberships
- American Society for Microbiology
- American Society for Biochemistry and Molecular Biology
Professional Activities
- Department of Biological Chemistry Retreat Committee, Co-Chair, 2017-present
- Department of Biological Chemistry Seminar Series, Chair, 2015-present
- Biological Chemistry Graduate Program Admissions Committee, Member, 2013-present
- Cross Disciplinary Gradate Program in Biomedical Sciences Admissions Committee, Member, 2018-present
- Immunology Gradate Program Admissions Committee, Member, 2019-2020
- Graduate Program in Biological Chemistry, Director, 2018 -present
- Johns Hopkins Bug Super Group, Co-Founder, 2017-present
- Society for Advancement of Chicanos/Hispanics and Native Americans in Science (SACNAS), Baltimore Chapter, Faculty Advisor, 2017-present
- Frontiers in Cellular and Infection Microbiology, Associate Editor, 2022-present
Additional Training
- Postdoctoral Fellowship, Tufts University School of Medicine, Boston, MA
Affiliation: Professor of Biological Chemistry
Description of Research
Research in the Gould lab is focused on the intersection of cell biology, bioengineering, and human disease.
Mechanisms of exosome biogenesis
Exosomes are small secreted vesicles of ~100 nm in size that play critical roles in human health and disease. We study the molecular mechanisms of exosome biogenesis by interrogating the biogenesis, intracellular trafficking, and vesicular secretion of highly enriched exosome cargo proteins, as well as viral proteins that use the hosts’ exosome biogenesis pathways for the formation of infectious viruses. Most recently, we’ve discovered that exosome marker proteins all bud primarily from the plasma membrane, and moreover, that endocytosis of exosome marker proteins from the plasma membrane greatly inhibits their vesicular secretion. These results re-write our understanding of exosome biogenesis by showing that it occurs primarily by direct budding from the plasma membrane, with only minor contributions from exocytosis of internal vesicles (Ai et al. Science Advances 2024, https://www.science.org/doi/10.1126/sciadv.adi9156).
Cell and exosome engineering
As the only bionormal nanovesicle, exosomes are an ideal delivery vehicle for vaccines, biologics, and drugs. Our laboratory uses our latest advances in exosome biogenesis to create proteins that are efficiently loaded into exosomes and confer unique properties on recombinantly engineered exosomes, including induction of immune responses, inhibition of angiogenesis, and other biomedically important activities. We then drive the high-level production of recombinant exosome-targeted proteins using new, highly restrictive antibiotic resistance genes that allow us to rapidly create cell lines that express the highest possible levels of recombinant proteins.
Synthetic signaling systems
Together with Dr. Michael Caterina’s lab, we’ve invented synthetic signaling systems that convert pathogenic signaling pathways into tunable, negative feedback loops that attenuate their pathogenic effects. These genetically-encoded tools are designed to ameliorate chronic diseases, with our primary focus on developing a safe and effective treatment for chronic pain.
Research Description
Bacteria are ubiquitous microorganisms that impact human health in myriad ways, including as pathogens and as commensal members of the microbiota. A fundamental understanding of the mechanisms of bacterial growth and adaptation is key to controlling their replication and survival. Our overarching research goal is to discover how bacteria grow, divide, and survive in diverse and potentially stressful environments. This is a particularly important goal as we confront the growing crisis in antimicrobial resistance.
Our laboratory takes a multi-faceted approach to study bacterial growth, incorporating cell biology, biochemistry, and genetic and genomic toolkits. We leverage two Gram-negative species: the free-living model Caulobacter crescentus and the obligate intracellular, tick-borne human pathogen Rickettsia parkeri. We take a comparative cell biology perspective to ask how growth, division, and adaptation of these two related bacteria has evolved to support survival in distinct growth environments.
NIH Bibliography page: https://www.ncbi.nlm.nih.gov/sites/myncbi/erin.goley.1/bibliography/50199813/public/
Current Lab Members
Name | Role |
---|---|
Wanda Figueroa-Cuilan, PhD | Postdoctoral Fellow |
Erika Smith | BCMB Graduate Student |
Trung Nguyen | BCMB Graduate Student |
Isaac Payne | BCMB Graduate Student |
Dezmond Cole | BCMB Graduate Student |
Publications (since joining Johns Hopkins)
Barrows JM, Anderson AS, Talavera-Figueroa BK and and Goley ED. (2023) Intrinsic and extrinsic factors regulate FtsZ function in Caulobacter crescentus. [pre-print] bioRxiv
Daitch AK and Goley ED. (2023) OpgH is an essential regulator of Caulobacter morphology. [pre-print] bioRxiv
Figueroa-Cuilan WM, Irazoki O, Feeley M, Smith E, Nguyen T, Cava F, Goley ED. (2023) Quantitative analysis of morphogenesis and growth dynamics in an obligate intracellular bacterium. MBoC. 34(7):ar69. (2023)
Barrows JM and Goley ED. (2023) Synchronized swarmers and sticky stalks: Caulobacter crescentus as a model for bacterial cell biology. J Bacteriology. e0038422.
Daitch AK, Orsburn BC, Chen Z, Alvarez L, Eberhard CD, Sundararajan K, Zeinert R, Kreitler DF, Jakoncic J, Chien P, Cava F, Gabelli SB, Goley ED. (2023) EstG is a novel esterase required for cell envelope integrity in Caulobacter. Current Biology. 33: 228-240. (2023)
Mahone CR, Yang X, McCausland JW, Payne IP, Xiao J, Goley ED. (2022) Integration of cell wall synthesis activation and chromosome segregation during cell division in Caulobacter. [pre-print] bioRxiv
Barrows JM and Goley ED. (2021) FtsZ dynamics in bacterial division: What, how, and why? Curr Opin Cell Biol. 68:163-172
Daitch AK and Goley ED. (2020) Uncovering unappreciated activities and niche functions of bacterial cell wall enzymes. Curr Biol. 30:R1170-R1175
Mahone CR and Goley ED. (2020) Bacterial Cell Division at a Glance. J Cell Science. 133: jcs237057 (2020)
Barrows JM*, Sundararajan K*, Bhargava A, Goley ED. (2020) FtsA Regulates Z-ring Morphology and Cell Wall Metabolism in an FtsZ C-terminal Linker Dependent Manner in C. crescentus. J Bacteriol. 202: e00693-19
Woldemeskel SA, Daitch AK, Alvarez L, Gaël Panis, Zeinert R, Gonzalez D, Smith E, Collier J, Chien P, Cava F, Viollier PH, Goley ED. (2020) The conserved transcriptional regulator CdnL is required for metabolic homeostasis and morphogenesis in Caulobacter. PLOS Genetics. 16: e1008591
Lariviere PJ, Mahone CR, Santiago-Collazo G, Howell M, Daitch AK, Zeinert R, Chien P, Brown PJB, Goley ED. (2019) An essential regulator of bacterial division links FtsZ to cell wall synthase activation. Current Biology. 29:1460-70
Howell ML, Aliaskevich A, Sundararajan K, Daniel JJ, Lariviere PJ, Goley ED, Cava F, Brown PJB. (2019) Agrobacterium tumefaciens divisome proteins regulate the transition from polar growth to cell division. Mol Micro. 111:1074-92
Sundararajan K, Vecchiarelli AG, Mizuuchi K, Goley ED. (2018) Species- and C-terminal linker-dependent variations in the dynamic behavior of FtsZ on membranes in vitro. Mol Micro. 110: 47-63
Lambert A, Vanhecke A, Archetti A, Holden S, Schaber F, Pincus Z, Laub MT, Goley ED, and Manley S. (2018) Constriction rate modulation can drive cell size control and homeostasis in C. crescentus. iScience. 4: 180-189
Lariviere PJ, Szwedziak P, Mahone CR, Löwe J, and Goley ED. (2018) FzlA, an essential regulator of FtsZ protofilament curvature, controls constriction rate during Caulobacter division. Mol Micro. 107: 180-197.
Sundararajan K and Goley ED. (2017) The intrinsically disordered C-terminal linker of FtsZ regulates protofilament dynamics and superstructure in vitro. J Biol Chem. 292:20509-20527.
Meier EL, Yao Q, Daitch AK, Jensen GJ, and Goley ED. (2017) FtsEX-mediated regulation of the final stages of cell division reveals morphogenetic plasticity in Caulobacter crescentus. PLoS Genetics. 13:e1006999.
Woldemeskel SA, McQuillen R, Hessel AM, Xiao J, and Goley ED (2017) A conserved coiled-coil protein pair focuses the cytokinetic Z-ring in Caulobacter crescentus. Mol Micro. 105:721-740.
Woldemeskel SA and Goley ED (2017) Shapeshifting to survive: shape determination and regulation in Caulobacter crescentus. Trends Microbiol. 25:673-687.
Sundararajan K and Goley ED (2017) Cytoskeletal proteins in Caulobacter crescentus: spatial orchestrators of cell cycle progression, development, and cell shape. Subcell Biochem. 84:103-137.
Xiao J and Goley ED. (2016) Redefining the roles of the FtsZ-ring in bacterial cytokinesis. Curr Opin Microbiol. 34:90-96.
Meier EL, Ravazi S, Inoue T, and Goley ED. (2016) A novel membrane anchor for FtsZ is linked to cell wall hydrolysis in Caulobacter crescentus. Mol Microbiol. 101:265-280.
Sundararajan K, Miguel A, Desmarais SM, Meier EL, Huang KC, and Goley ED. (2015) The bacterial tubulin FtsZ requires its intrinsically disordered linker to direct robust cell wall construction. Nat Commun. 6:7281.
Meier EL and Goley ED. (2014) Form and function of the bacterial cytokinetic ring. Curr Opin Cell Biol. 26:19-27.
Goley ED. (2013) Tiny cells meet big questions: a closer look at bacterial cell biology. Mol Biol Cell. 24:1099-102.