Several themes, one lens:
Bacteria don't live in flasks. They navigate physical barriers, compete with neighboring microbes, and constantly fend off viral and immunological predators, all while trying to infect and colonize us. Our research is organized around several interconnected lines of inquiry, united by a single question: what are the rules of bacterial survival, and how do we use those rules to defeat them?
Bacterial Organization & MechanomicrobiologyBacteria are far more structurally sophisticated than classical models suggested. We discovered how bacteria build cytoskeletons, sculpt their shapes, and sense mechanical forces like fluid flow and surface stiffness, as well as how this physical organization directly regulates virulence. This work helped establish the field of mechano-microbiology: bacteria both use mechanics to shape themselves and actively read their mechanical environment as a core part of how they cause disease. Bartlett et al., Cell 2017 · CrvA links V. cholerae morphology to pathogenesis |
Single-Cell Heterogeneity & Host InteractionsBacteria within a clonal population are not identical. Individual cells harbor striking differences in gene expression that determine which ones survive antibiotic treatment, which ones successfully infect a host, and which ones are killed by phages. We developed M3-Seq and Duet-Seq as massively parallel single-cell RNA sequencing platforms to reveal how this individuality shapes bacterial outcomes in ways that bulk measurements entirely miss. Wang et al., Nature Microbiology 2023 · M3-Seq identifies rare antibiotic-surviving subpopulations and single-cell phage responses |
Phage-Bacteria Conflict & Anti-Infective DiscoveryBacteria are not only predators but are prey. We study the regulatory principles of phage-bacteria conflict: how phages recognize and kill bacteria, how bacteria defend themselves, and how these dynamics unfold in 3D environments that better resemble real infections. These same principles guide our therapeutic work: using imaging-based machine learning, we have discovered antibiotics with novel mechanisms that evade resistance entirely as well as novel antibiotics whose spectrum can be tuned from broad to narrow spectrum to selectively spare the host microbiome. Martin et al., Cell 2020 · SCH-79797, dual-mechanism antibiotic that avoids resistance |
Recent Publications
Contact
Gitai Lab
Department of Molecular Biology
Princeton University
355 Thomas Laboratory
Washington Road
Princeton, NJ 08544
p 609-258-9420
Faculty Assistant
Ellen Brindle-Clark
[email protected]
230 Thomas Laboratory
p 609-258-5419
f 609-258-6175
Lab Website
scholar.princeton.edu/gitailab