Persisters are bacterial cells able to survive killing by antibiotics. This antibiotic tolerance is mechanistically distinct from resistance. Persisters are not mutants but phenotypic variants.

We are interested in genetic mechanism(s) underlying formation of persister fraction within genetically identical antibiotic-susceptible population of bacteria. Understanding these mechanisms is important in order to get a complete and realistic picture of pathogens during the infection and antibiotic treatement, especially in the case of chronic and relapsing infections. In addition there is an interest in uncovering the mechanism of generation of phenotypic diversity and its role and significance in evolution.

Current projects involve isolation and characterization of high persistence mutants in Escherichia coli and Yersinia pestis, characterization of E. coli knock-out mutants exhibiting low persistence phenotype, the link between stress responses (SOS and heat shock) and persistence and the role of recombination and SOS-functions in persistance to fluoroquinolones.