Persisters are a subpopulation of normal bacterial cells that are tolerant to antibiotics without a dedicated resistance mechanism. Previously, it has been demonstrated that high persister mutants are selected for in vivo, which may indicate a contribution to chronic infections in human disease. The mechanisms of persister formation are highly redundant and not fully understood. Toxin-antitoxin (TA) modules have been implicated in the formation of persisters. Typically, a stable toxin and unstable antitoxin are bound in an inactive state inside the cell. Under stress, the unstable antitoxin is degraded, releasing the toxin which inhibits growth. My project focuses on the eleven TA interferases found in Escherichia coli. Interferases degrade mRNA in the cell. I am utilizing fluorescent activated cell sorting (FACS) to investigate the heterogenous expression of these toxins in a wild type population and their contribution to the persister phenotype. One such TA interferase is mqsRA. In previous studies, it was found that mqsRA is more highly expressed in persisters versus non-persisters. Artificial over-expression of mqsRA led to a 10,000-100,000 fold increase in persisters. Taken together, these data suggest a role for MqsR in persister formation. Interestingly, my results reveal that sorting high, medium, and low levels of mqsRA expressing cells from a wild-type population exhibited similar levels of persistence to fluoroquinolones. This may indicate that MqsR has little effect on the persister phenotype under these conditions or perhaps posttranslational regulation of MqsR is more important than transcription of the mqsRA. Experiments are underway to further investigate these possibilities.