Greater Boston
My project focused on how bacterial cells adapt to host-imposed stress, using Neisseria gonorrhoeae as a model to investigate transcriptional regulation under conditions such as iron limitation and oxidative stress. I characterized the role of MpeR, an AraC-family regulator, in mediating stress responses during infection, and applied RNA-seq, gene knockouts, co-expression network analysis, and host-cell assays to define its regulatory targets and physiological impact. This work contributes to a broader understanding of how bacterial regulatory networks govern survival, resistance, and host interaction under dynamic environmental conditions. Prior to graduate school, I contributed to research across cancer genomics, virology, and immunology. At Dana-Farber Cancer Institute, I helped develop next-generation sequencing workflows and contributed to multiple clinically relevant cancer sequencing studies. At UMass Medical School, I investigated mechanisms of influenza A virus adaptation to antiviral pressure, including cap-snatching and RNA replication dynamics. My early work at UT Southwestern examined chemokine regulation in a mouse model of lupus. Across these diverse systems, I’ve consistently applied molecular biology, transcriptomics, and systems-level tools to understand how cells regulate their behavior in complex biological contexts.
Neisseria gonorrhoeae is the etiological agent of the sexually transmitted infection (STI) gonorrhea, a high morbidity disease worldwide with ~ 106 million cases annually. Like many human pathogens this organism must adapt to environments encountered during infection, including low pH and varying oxygen and iron levels. Tight control of gene expression in the gonococcus is mediated in part by the Fur protein, which binds to specific DNA sequences leading to either activation or repression of a repertoire of genes. Our lab recently reported that the gonococcal Fur regulon extends to additional regulatory proteins, which together contribute to gonococcal mechanisms of pathogenesis. We also established that subsets of Fur regulated genes are expressed during natural gonococcal infection in men and women relative to during growth in vitro. My project involves studying these novel Fur regulatory networks expressed and regulated in the human genital tract and defining their contribution to natural infection.
• Designed and executed multifactor, time-resolved RNA-seq experiments to investigate transcriptional regulation and stress adaptation in Neisseria gonorrhoeae under iron-replete and iron-depleted conditions. • Analyzed transcriptomic datasets using differential expression, time-course analysis, and operon-level interpretation to characterize dynamic bacterial stress responses. • Developed and applied gene regulatory network and module-level analyses to identify candidate regulators associated with iron homeostasis, oxidative stress, and metabolic adaptation. • Integrated transcriptomic findings with phenotypic assays, including growth, viability, oxidative stress tolerance, and epithelial cell invasion experiments, to connect molecular regulation with bacterial behavior. • Performed motif discovery and computational regulatory analysis to prioritize putative transcriptional relationships and biologically relevant targets. • Generated publication-style visualizations and analytical summaries to communicate complex multi-layer datasets and support biological interpretation.
Influenza A Virus cap-snatching
Studied Influenza A virus cap-snatching and RNA replication mechanisms. Conducted mutagenesis, qPCR, and viral replication assays.
Next Generation Sequencing. Cancer Research