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金黄色葡萄球菌膜泡中镉和锰的转运

Cadmium and manganese transport in Staphylococcus aureus membrane vesicles.

作者信息

Perry R D, Silver S

出版信息

J Bacteriol. 1982 May;150(2):973-6. doi: 10.1128/jb.150.2.973-976.1982.

DOI:10.1128/jb.150.2.973-976.1982
PMID:7068540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC216454/
Abstract

The presence of plasmid gene cadB did not affect Cd2+ accumulation, whereas plasmid gene cadA reduced Cd2+ accumulation by whole cells but not by membrane vesicles. Membrane vesicle studies indicated that Cd2+ uptake occurred via the Mn2+ transport system which was energized by the membrane electrical potential. Mn2+ and Cd2+ were competitive inhibitors of each other's transport, with Km's of 0.95 microM Mn2+ and 0.2 microM Cd2+. The kinetic parameters were nearly identical with vesicles prepared from sensitive and resistant cells, indicating that the cadA-encoded Cd2+ efflux system was inoperative in membrane vesicle preparations. Experiments with energy-inhibited cells indicated that the cadB gene product may bind Cd2+.

摘要

质粒基因cadB的存在并不影响Cd2+的积累，而质粒基因cadA可降低全细胞对Cd2+的积累，但对膜泡无此作用。膜泡研究表明，Cd2+通过由膜电位供能的Mn2+转运系统进入细胞。Mn2+和Cd2+是彼此转运的竞争性抑制剂，Mn2+的Km值为0.95微摩尔，Cd2+的Km值为0.2微摩尔。敏感细胞和抗性细胞制备的膜泡的动力学参数几乎相同，这表明cadA编码的Cd2+外排系统在膜泡制备中不起作用。对能量抑制细胞的实验表明，cadB基因产物可能与Cd2+结合。

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Reduced cadmium transport determined by a resistance plasmid in Staphylococcus aureus.金黄色葡萄球菌中一种耐药质粒所决定的镉转运减少。
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