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.
