Selifonova O V, Barkay T
Center for Environmental Diagnostics and Bioremediation, University of West Florida, Gulf Breeze.
Appl Environ Microbiol. 1994 Oct;60(10):3503-7. doi: 10.1128/aem.60.10.3503-3507.1994.
The effects of sodium ions on the uptake of Hg2+ and induction of the Tn21 mer operon were studied by using Escherichia coli HMS174 harboring the reporter plasmids pRB28 and pOS14. Plasmid pRB28 carries merRT', and pOS14 carries merRTPC of the mer operon, both cloned upstream of a promoterless luciferase gene cassette in pUCD615. The bioluminescent response to 1 microM Hg2+ was significantly inhibited in E. coli HMS174(pRB28) in minimal medium supplemented with sodium ions at 10 to 140 mM. After initial acceleration, light emission declined at 50 nM Hg2+ in the presence of Na+. The mer-lux assay with resting cells carrying pRB28 and 203Hg2+ uptake experiments showed increased induction and enhanced mercury uptake, respectively, in media supplemented with sodium ions. The presence of Na+ facilitated maintenance of bioluminescence in resting HMS174(pRB28) cells induced with 50 nM Hg2+. External K+ stimulated bioluminescent response in HMS174(pRB28) and HMS174(pOS14) grown in sodium phosphate minimal medium devoid of potassium ions. Sodium ions appear to facilitate mercury transport. We propose that sodium-coupled transport of mercuric ions can be one of the mechanisms for mercury uptake by E. coli and that the Na+ gradient may energize the transport of Hg2+.
利用携带报告质粒pRB28和pOS14的大肠杆菌HMS174，研究了钠离子对Hg2+摄取和Tn21 mer操纵子诱导的影响。质粒pRB28携带merRT'，pOS14携带mer操纵子的merRTPC，二者均克隆于pUCD615中无启动子的荧光素酶基因盒的上游。在添加了10至140 mM钠离子的基本培养基中，大肠杆菌HMS174(pRB28)对1 microM Hg2+的生物发光反应受到显著抑制。在有Na+存在的情况下，初始加速后，50 nM Hg2+时发光强度下降。对携带pRB28的静息细胞进行mer-lux检测以及203Hg2+摄取实验表明，在添加了钠离子的培养基中，诱导作用增强，汞摄取增加。Na+的存在有助于维持用50 nM Hg2+诱导的静息HMS174(pRB28)细胞中的生物发光。外部K+刺激了在不含钾离子的磷酸钠基本培养基中生长的HMS174(pRB‘)和HMS174(pOS14)的生物发光反应。钠离子似乎促进汞的运输。我们提出，汞离子的钠偶联运输可能是大肠杆菌摄取汞的机制之一，并且Na+梯度可能为Hg2+的运输提供能量。
