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Bacterial persister cells, tolerant to antibiotics, may arise from the HipBA toxin-antitoxin system. A new model shows this system

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Area of Science:

  • Microbiology
  • Bacterial Physiology
  • Systems Biology

Background:

  • Persister cells are a small subpopulation of bacteria exhibiting increased tolerance to antibiotics.
  • Toxin-antitoxin modules, such as HipBA in Escherichia coli, are implicated in the formation of persister cells.
  • The HipA7 allele is a well-characterized high-persistence mutant.

Purpose of the Study:

  • To develop a stochastic model for the HipBA system to explain bistability.
  • To investigate the role of reciprocal coupling between free HipA and cellular growth rate in persistence.
  • To understand the mechanisms underlying the transition between active and dormant states in persister cells.

Main Methods:

  • Development of a stochastic model for the HipBA toxin-antitoxin system.
  • Mathematical modeling of the reciprocal coupling between free HipA and cellular growth rate.
  • Comparison of model predictions with experimental data from synthetic promoter constructs.

Main Results:

  • The stochastic model successfully generates bistability in the HipBA system.
  • The model demonstrates that reciprocal coupling of free HipA to cellular growth rate drives bistability.
  • The actively growing and dormant states correspond to stable states within the model.
  • Stochastic fluctuations facilitate transitions between the active and dormant states.

Conclusions:

  • The HipBA system can generate bistability, leading to the formation of persister cells.
  • Cellular growth rate plays a crucial role in regulating the transition between active and dormant states.
  • The developed stochastic model accurately reflects experimental observations of bacterial persistence.