Abstract
BackgroundPersistence is a natural phenomenon whereby a subset of a population of isogenic bacteria either grow slow or become dormant conferring them with the ability to withstand various stresses including antibiotics. In a clinical setting bacterial persistence often leads to the recalcitrance of various infections increasing the treatment time and cost. Additionally, some studies also indicate that persistence can also pave way for the emergence of resistant strains. In a laboratory setting this persistent phenotype is enriched in nutritionally deprived environments. Consequently, in a batch culture the late stationary phase is enriched with persistent bacteria. The mechanism of persister cell formation and its regulation is not well understood. Toxin-antitoxin (TA) systems have been implicated to be responsible for bacterial persistence and rifampicin is used to treat highly persistent bacterial strains. The current study tries to explore a possible interaction between rifampicin and the MazEF TA system that furthers the former’s success rate in treating persistent bacteria.ResultsIn the current study we found that the population of bacteria in the death phase of a batch culture consists of metabolically inactive live cells resembling persisters, which showed higher membrane depolarization as compared to the log phase bacteria. We also observed an increase in the expression of the MazEF TA modules in this phase. Since rifampicin is used to kill the persisters, we assessed the interaction of rifampicin with MazEF complex. We showed that rifampicin moderately interacts with MazEF complex with 1:1 stoichiometry.ConclusionOur study suggests that the interaction of rifampicin with MazEF complex might play an important role in inhibition of persisters.
Highlights
Persistence is a natural phenomenon whereby a subset of a population of isogenic bacteria either grow slow or become dormant conferring them with the ability to withstand various stresses including antibiotics
In this study we showed that MazEF expression is induced during the late phase of bacterial growth and rifampicin directly interacts with MazEF complex
E. coli death phase population consists of live cells that are metabolically inactive In a batch culture, a typical bacterial growth curve consists of 5 distinct phases, i.e., lag phase, exponential phase, stationary phase, death phase and followed by a long-term stationary phase that is maintained for years [13]
Summary
Persistence is a natural phenomenon whereby a subset of a population of isogenic bacteria either grow slow or become dormant conferring them with the ability to withstand various stresses including antibiotics. The mechanism of persister cell formation and its regulation is not well understood. The current study tries to explore a possible interaction between rifampicin and the MazEF TA system that furthers the former’s success rate in treating persistent bacteria. Persisters represent a subset of a population of isogenic bacteria that are characterized by reduced or no growth, thereby helping the bacterial population tide over stressful situations including antibiotics [1]. Alexander et al BMC Molecular and Cell Biology (2020) 21:73 antibiotics which suggests that the late stationary phase bacteria behave as natural persisters. Studies suggest that MazEF plays a significant role in bacterial persistence. ClpP and Lon proteases, which degrade MazE, when deleted led to the decrease in persister population [9]
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