Formycin A resistant mutants due to defect in adenosine transport system in Vibrio parahaemolyticus

Y Sakai-Tomita1, Y Mitani, M Tsuda

  • 1Department of Microbiology, Faculty of Pharmaceutical Sciences, Okayama University, Japan.

Insights

Formycin A, an antibiotic, inhibits Vibrio parahaemolyticus growth by entering cells via the sodium-coupled adenosine transporter. Mutants defective in this transporter are resistant to formycin A.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • Formycin A is an antibiotic known to inhibit the growth of certain bacteria, including Vibrio parahaemolyticus.
  • Previous research identified a sodium (Na+)-coupled cotransport system responsible for adenosine uptake in Vibrio parahaemolyticus.

Purpose of the Study:

  • To investigate the mechanism of formycin A uptake in Vibrio parahaemolyticus.
  • To determine if formycin A utilizes the previously identified adenosine transport system.
  • To characterize formycin A resistant mutants and their relation to the adenosine transport system.

Main Methods:

  • Isolation and characterization of formycin A resistant mutants.
  • Growth assays of mutants on adenosine as a sole carbon source.
  • Measurement of 14C-adenosine uptake and Na+ uptake in response to adenosine or formycin A.

Main Results:

  • Formycin A uptake was mediated by the Na+-coupled adenosine transport system.
  • Approximately half of the isolated formycin A resistant mutants exhibited poor growth on adenosine.
  • These mutants showed abolished Na+ uptake and respiration-driven 14C-adenosine uptake, indicating a defect in the Na+/adenosine cotransport system.

Conclusions:

  • The Na+/adenosine cotransport system is responsible for formycin A uptake in Vibrio parahaemolyticus.
  • Mutations in the Na+/adenosine cotransport system confer resistance to formycin A.
  • This study elucidates the transport mechanism of an antibiotic and provides insights into bacterial nutrient transport systems.

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