Growth control switch by a DNA-damage-inducible toxin-antitoxin system in Caulobacter crescentus

Clare L Kirkpatrick1, Daniel Martins1, Peter Redder1

  • 1Department of Microbiology &Molecular Medicine, Institute of Genetics &Genomics in Geneva (iGE3), Faculty of Medicine/CMU, University of Geneva, Rue Michel-Servet 1, 1211 Genève 4, Switzerland.

Nature Microbiology
|August 31, 2016
PubMed

Insights

Bacterial toxin-antitoxin systems (TASs) can switch between promoting and inhibiting bacterial growth. This outcome switching depends on toxin dosage and mRNA targets, influencing stress response and cell cycle networks.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Bacterial toxin-antitoxin systems (TASs) are crucial for stress response, often inducing growth arrest via toxin-mediated RNA cleavage.
  • The precise mRNA targets and regulatory roles of many TASs remain unclear, hindering their integration into cellular networks.

Purpose of the Study:

  • To investigate the regulatory role and target specificity of the HigBA toxin-antitoxin system in Caulobacter crescentus.
  • To determine how HigB toxin dosage and mRNA targets influence bacterial growth and cellular processes.

Main Methods:

  • Analysis of the HigBA toxin-antitoxin system in Caulobacter crescentus.
  • Investigating the impact of HigB toxin dosage and LexA regulation on bacterial growth.
  • Identifying mRNA targets of HigB's RNA cleavage activity.

Main Results:

  • The HigBA system exhibits outcome-switching activity, promoting or inhibiting bacterial growth based on HigB dosage.
  • HigB is regulated by the DNA damage (SOS) repressor LexA, in addition to its antitoxin HigA.
  • HigB targets specific mRNAs, including an efflux pump, affecting cell viability and cell cycle progression.

Conclusions:

  • Bacterial toxin-antitoxin systems can exhibit dynamic regulatory roles, influencing both stress adaptation and fundamental cellular processes like the cell cycle.
  • Understanding TAS target selectivity is key to deciphering their integration into complex bacterial regulatory networks.

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