Helbig Kerstin, Bleuel Corinna, Krauss Gerd J, Nies Dietrich H
Institute for Biology, Life Science Faculty, Martin-Luther-University Halle-Wittenberg, Kurt-Mothes-Str 3, 06099 Halle, Germany.
J Bacteriol. 2008 Aug;190(15):5431-8. doi: 10.1128/JB.00271-08. Epub 2008 Jun 6.
Glutathione (GSH) and its derivative phytochelatin are important binding factors in transition-metal homeostasis in many eukaryotes. Here, we demonstrate that GSH is also involved in chromate, Zn(II), Cd(II), and Cu(II) homeostasis and resistance in Escherichia coli. While the loss of the ability to synthesize GSH influenced metal tolerance in wild-type cells only slightly, GSH was important for residual metal resistance in cells without metal efflux systems. In mutant cells without the P-type ATPase ZntA, the additional deletion of the GSH biosynthesis system led to a strong decrease in resistance to Cd(II) and Zn(II). Likewise, in mutant cells without the P-type ATPase CopA, the removal of GSH led to a strong decrease of Cu(II) resistance. The precursor of GSH, gamma-glutamylcysteine (gammaEC), was not able to compensate for a lack of GSH. On the contrary, gammaEC-containing cells were less copper and cadmium tolerant than cells that contained neither gammaEC nor GSH. Thus, GSH may play an important role in trace-element metabolism not only in higher organisms but also in bacteria.
谷胱甘肽(GSH)及其衍生物植物螯合肽是许多真核生物中过渡金属稳态的重要结合因子。在此,我们证明GSH也参与大肠杆菌中铬酸盐、锌(II)、镉(II)和铜(II)的稳态及抗性。虽然合成GSH能力的丧失对野生型细胞的金属耐受性影响甚微,但GSH对没有金属外排系统的细胞的残余金属抗性很重要。在没有P型ATP酶ZntA的突变细胞中,GSH生物合成系统的额外缺失导致对镉(II)和锌(II)的抗性大幅下降。同样,在没有P型ATP酶CopA的突变细胞中,去除GSH导致对铜(II)的抗性大幅下降。GSH的前体γ-谷氨酰半胱氨酸(γEC)无法弥补GSH的缺乏。相反,含有γEC的细胞比既不含γEC也不含GSH的细胞对铜和镉的耐受性更低。因此,GSH可能不仅在高等生物中,而且在细菌的微量元素代谢中都发挥着重要作用。