Georgiana Purdy earned her bachelor’s degrees in Microbiology and Cell Science (BS, with honors) and History (BA, with honors) from the University of Florida in 1998. She subsequently obtained her Ph.D. from the University of Texas at Austin in 2003, working with Dr. Shelley Payne on the bacterial pathogen Shigella flexneri. Specifically, her thesis project focused on the role of S. flexneri periplasmic chaperones in virulence and the extracytoplasmic stress response. She then performed her postdoctoral training with Dr. David Russell at Cornell University, where she studied the host-pathogen interface between Mycobacterium tuberculosis and the macrophage. Her postdoctoral research demonstrated that the mycobactericidal properties of macrophages include the delivery of bacteria to a hydrolytic lysosome enriched in bactericidal Ub-peptides (Alonso et al., 2007). This novel insight dramatically impacted the field’s understanding of how M. tuberculosis was killed by activated and autophagic macrophages.

Dr. Purdy joined the OHSU MMI Department in 2008 as an Assistant Professor and established her independent research program focused on M. tuberculosis. The goals of the Purdy Lab are to further define the intrinsic resistance of the pathogen to the host immune response and antibiotics, delineate pathways in mycobacterial cell wall biogenesis, and identify targets and new strategies for future drug therapy. The lab combines the approaches of bacterial genetics, biochemistry and cell biology to achieve these goals. 

Current efforts in the Purdy lab are focused on characterizing the function and regulation of mycobacterial MmpL cell wall lipid transporters that are crucial contributors to mycobacterial physiology and pathogenesis. Our focus is on MmpL11, which is conserved in non-pathogenic and pathogenic mycobacteria. MmpL11 plays a conserved role in mycobacterial biofilm formation. We have identified the lipids transported by MmpL11 as monomeromycolyl diacylglycerol (MMDAG), long chain TAGs, and mycolate wax ester (MWE). These lipids have been classified as “storage lipids” and are implicated in non-replicating persistence or latency. Consistent with this role, we showed that the M. tuberculosis mmpL11 mutant is impaired for survival and/or resuscitation compared to wild-type M. tuberculosis when incubated under nutrient and oxygen starvation. Furthermore, we showed that the mmpL11 mutant is less fit than wild-type in an in vitro granuloma model. Combined these data suggest that MmpL11 and its substrates are important for M. tuberculosis non-replicating persistence and latency.

Dr. Purdy became an Associate Professor in 2014 and received tenure in 2016. Work in the Purdy lab is funded by the NIH.