Wendy Mok, PhD

Our research focuses on how bacteria respond to and survive antibiotic treatment. We are especially interested in bacterial persisters, which are rare cell types in a population that can tolerate lethal doses of antibiotics that kill their genetically identical kin. Unlike antibiotic resistant mutants, persisters have not acquired heritable genetic changes that allow them to grow in the presence of antibiotics. Rather, the persister phenotype is transient. Once the antibiotic is removed and cells resume growth, the phenotype is lost. As persisters are recalcitrant to antibiotic treatment, they can potentially fuel the development of relapsing chronic infections and antibiotic resistance. Our major goal is to understand the triggers and survival strategies of bacterial persisters. We use genetic, biochemical, and systems biology approaches to investigate how fluctuations in the host environment impact persistence and how bacteria respond to and recover from treatment with antibiotics that target different cellular components. Contact us to find out more.

Stationary-phase Pseudomonas aeruginosa fluoroquinolone persisters mostly avoid DNA double-stranded breaks. Time-Lapse Epifluorescence Microscopy Imaging of Pseudomonas aeruginosa and Staphylococcus aureus Heterogeneous Phenotypes. Metabolites augment oxidative stress to sensitize antibiotic-tolerant Staphylococcus aureus to fluoroquinolones. Agar and agarose used for Staphylococcus aureus biofilm cultivation impact fluoroquinolone tolerance. Metabolic and transcriptional activities underlie stationary-phase Pseudomonas aeruginosa sensitivity to Levofloxacin. Stimulating Transcription in Antibiotic-Tolerant Escherichia coli Sensitizes It to Fluoroquinolone and Nonfluoroquinolone Topoisomerase Inhibitors. Probiotic Escherichia coli Nissle 1917 Inhibits Bacterial Persisters that Survive Fluo