View of Lake Mendota from Microbial Sciences Building
Microscopy image of red and green cells
Microscopy image of cells with red cell walls and blue DNA
Superhero labelled DksA prevents collision between RNA polymerase and DNA polymerase trains
Microscopy image of cells with red cell walls and internal green foci
Diagram of control of replication-transcription conflict and resulting response and plates with B. subtilis colonies
B. subtilis stringent response
Rack of test tubes with Jade and Christina working in background
Microscopy images of red and green cells (left) and blue cells with foci at septa (right)
Lab members in PPE
12 plates of cupcakes in varying colors

Bacterial stress responses allow cells to survive fluctuating environments, antibiotic treatments, and host defenses. While the transcriptional and post-transcriptional networks governing stress responses have been characterized extensively, there are major gaps in our knowledge beyond transcription regulation. My current research aims to answer the following fundamental questions: How do bacteria utilize stress-induced small molecules to adapt to their specific environmental niches? How do bacteria enter a metabolically dormant persister state that is intrinsically tolerant to a broad array of antibiotic treatments? How do stressed bacteria mitigate potential conflicts between their DNA replication and transcription machineries to ensure survival? What are the molecular mechanisms of bacterial evolution to fit their specific niches? We combine metabolomics, transcriptomics, and proteomics with biochemical and evolutionary approaches to answer these questions.  We study these processes in the Gram-positive bacterium Bacillus subtilis and the Gram-negative bacterium Escherichia coli. These organisms grow fast and are highly amenable to genetic manipulation. Because the fundamentals of information processing mechanisms are conserved across all domains of life, our work in bacteria is broadly applicable to other, less tractable, systems.