Formycin A resistant mutants due to defect in adenosine transport system in Vibrio parahaemolyticus.
An antibiotic formycin A inhibited growth of Vibrio parahaemolyticus under certain conditions, which suggested that formycin A was taken up by cells under these conditions. We found that formycin A was transported via the adenosine transport system which we previously reported as a Na(+)-coupled cotransport system. We isolated many formycin A resistant mutants, and about half of them grew very poorly on adenosine as a sole source of carbon. Judging from their reversion frequencies, these mutants seemed to have single mutations. Respiration driven uptake of 14C-adenosine was not observed in such mutants; also, Na+ uptake induced by the addition of adenosine or formycin A to a cell suspension was completely abolished in them. Thus we conclude that these mutants possess a defect in the Na+/adenosine cotransport system, and have become formycin A resistant.
Sakai-Tomita
Y
Y
Department of Microbiology, Faculty of Pharmaceutical Sciences, Okayama University, Japan.
Mitani
Y
Y
Tsuda
M
M
Tsuchiya
T
T
D000241:Adenosine / Q000378:metabolism*; D001693:Biological Transport, Active / Q000187:drug effects; D004352:Drug Resistance, Microbial; D005573:Formycins / Q000494:pharmacology*; D009154:Mutation; D014736:Vibrio parahaemolyticus / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism
D005573:Formycins; C034550:formycin; D000241:Adenosine