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High-throughput Screening of Chemical Compounds to Elucidate Their Effects on Bacterial Persistence
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HokB Monomerization and Membrane Repolarization Control Persister Awakening.
Dorien Wilmaerts1, Liselot Dewachter1, Pieter-Jan De Loose1
1Center for Microbiology, VIB, 3001 Leuven, Belgium; Centre of Microbial and Plant Genetics, KU Leuven, 3001 Leuven, Belgium.
Molecular Cell
|July 23, 2019
Summary
Bacterial persister cells, key to chronic infections, awaken from dormancy. This study reveals how the toxin HokB is disassembled, allowing membrane repolarization and regrowth, offering insights into antibiotic tolerance.
Area of Science:
- Microbiology
- Bacterial Physiology
- Infectious Diseases
Background:
- Bacterial persisters are subpopulations tolerant to antibiotics, contributing to chronic infection persistence.
- Persister cell awakening mechanisms remain poorly understood, hindering treatment strategies.
Purpose of the Study:
- To elucidate the molecular mechanisms governing the awakening of HokB-induced persister cells.
- To understand how persister cells transition from a dormant, tolerant state back to active growth.
Main Methods:
- Investigated the role of oxidoreductases DsbA and DsbC in HokB function.
- Utilized genetic and biochemical approaches to study HokB dimerization, monomerization, and degradation.
- Assessed membrane potential and ATP levels to monitor persister cell activity.
Main Results:
- HokB dimerization by DsbA is crucial for pore formation and stability in persister cells.
- DsbC-mediated monomerization triggers HokB degradation by DegQ, leading to pore disassembly.
- Pore disassembly restores membrane potential, enabling the electron transport chain to resume growth.
Conclusions:
- The DsbA/DsbC/DegQ system orchestrates the timely awakening of HokB-induced persister cells.
- Understanding persister cell awakening provides novel targets for combating chronic bacterial infections.
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