RNA chaperone hfq mediates persistence to multiple antibiotics in Aeromonas veronii

Lin Zhang1, Wenjing Yu1, Yanqiong Tang1

  • 1Key Laboratory of Tropical Biological Resources of Ministry of Education, School of Life Sciences and Pharmacy, Hainan University, 570228, Haikou, China.

Insights

The RNA-binding protein Hfq is crucial for antibiotic tolerance and persister formation in Aeromonas veronii. Deleting hfq in this fish pathogen significantly reduced its growth, antibiotic resistance, and persistence.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Pathogenic *Aeromonas veronii* causes significant health and economic losses in fish and humans.
  • Bacterial persister cells, exhibiting multiple drug tolerance, are a major cause of recurrent infections.
  • The ubiquitous RNA-binding protein Hfq is implicated in antibiotic tolerance and persister production.

Purpose of the Study:

  • To investigate the role of Hfq in *Aeromonas veronii*.
  • To determine the impact of *hfq* deletion on antibiotic tolerance and persister formation.
  • To elucidate the molecular mechanisms underlying Hfq-mediated effects.

Main Methods:

  • Gene deletion of *hfq* in *Aeromonas veronii*.
  • Assessment of bacterial growth rates.
  • Evaluation of antibiotic tolerance and persister cell formation.
  • Quantitative gene expression analysis (qRT-PCR) for key regulatory genes.

Main Results:

  • Deletion of *hfq* in *A. veronii* significantly retarded bacterial growth.
  • The *hfq* deletion mutant exhibited reduced tolerance to various antibiotics.
  • Persistence levels were significantly lowered in the absence of functional Hfq.
  • Downregulation of *relE*, *cspD*, *clpB*, *rpoS*, and *oxyR*, and upregulation of *oppB* were observed in the *hfq* deletion mutant.

Conclusions:

  • Hfq plays a critical role in promoting antibiotic tolerance and persister formation in *Aeromonas veronii*.
  • The observed effects are likely mediated by Hfq's regulation of specific genes involved in stress response and survival.
  • Understanding Hfq's function provides potential targets for combating recalcitrant *A. veronii* infections.

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