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副溶血性弧菌中由于腺苷转运系统缺陷导致的抗间型霉素A突变体。

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

作者信息

Sakai-Tomita Y, Mitani Y, Tsuda M, Tsuchiya T

机构信息

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

出版信息

Chem Pharm Bull (Tokyo). 1991 May;39(5):1325-7. doi: 10.1248/cpb.39.1325.

Abstract

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.

摘要

抗生素阿霉素A在某些条件下可抑制副溶血性弧菌的生长,这表明在这些条件下细胞摄取了阿霉素A。我们发现阿霉素A是通过我们之前报道的作为Na⁺偶联共转运系统的腺苷转运系统进行转运的。我们分离出了许多对阿霉素A耐药的突变体,其中约一半在以腺苷作为唯一碳源时生长非常差。从它们的回复频率判断,这些突变体似乎具有单个突变。在这些突变体中未观察到呼吸驱动的¹⁴C - 腺苷摄取;此外,向细胞悬液中添加腺苷或阿霉素A诱导的Na⁺摄取在它们中也完全被消除。因此我们得出结论,这些突变体在Na⁺/腺苷共转运系统中存在缺陷,并已对阿霉素A产生耐药性。

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