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在古菌嗜热硫磺酸中,MerH 在汞抗性中的作用。

Role of MerH in mercury resistance in the archaeon Sulfolobus solfataricus.

机构信息

School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68508, USA.

出版信息

Microbiology (Reading). 2013 Jun;159(Pt 6):1198-1208. doi: 10.1099/mic.0.065854-0. Epub 2013 Apr 25.

Abstract

Crenarchaeota include extremely thermoacidophilic organisms that thrive in geothermal environments dominated by sulfidic ores and heavy metals such as mercury. Mercuric ion, Hg(II), inactivates transcription in the crenarchaeote Sulfolobus solfataricus and simultaneously derepresses transcription of a resistance operon, merHAI, through interaction with the MerR transcription factor. While mercuric reductase (MerA) is required for metal resistance, the role of MerH, an adjacent small and predicted product of an ORF, has not been explored. Inactivation of MerH either by nonsense mutation or by in-frame deletion diminished Hg(II) resistance of mutant cells. Promoter mapping studies indicated that Hg(II) sensitivity of the merH nonsense mutant arose through transcriptional polarity, and its metal resistance was restored partially by single copy merH complementation. Since MerH was not required in vitro for MerA-catalysed Hg(II) reduction, MerH may play an alternative role in metal resistance. Inductively coupled plasma-mass spectrometry analysis of the MerH deletion strain following metal challenge indicated that there was prolonged retention of intracellular Hg(II). Finally, a reduced rate of mer operon induction in the merH deletion mutant suggested that the requirement for MerH could result from metal trafficking to the MerR transcription factor.

摘要

泉古菌包括极其嗜热嗜酸的生物体,它们在以硫化物矿石和重金属(如汞)为主的地热环境中茁壮成长。汞离子(Hg(II))可使嗜热古菌 Sulfolobus solfataricus 的转录失活,并通过与 MerR 转录因子相互作用同时解除抗性质粒 merHAI 的转录抑制。虽然汞还原酶(MerA)是金属抗性所必需的,但相邻的 ORF 小预测产物 MerH 的作用尚未得到探索。MerH 的无义突变或框内缺失会降低突变细胞对 Hg(II)的抗性。启动子图谱研究表明,merH 无义突变体对 Hg(II)的敏感性是通过转录极性引起的,其金属抗性可通过 merH 单拷贝的部分互补得到部分恢复。由于 MerH 在体外对 MerA 催化的 Hg(II)还原不是必需的,因此 MerH 可能在金属抗性中发挥替代作用。金属胁迫后对 MerH 缺失菌株进行电感耦合等离子体质谱分析表明,细胞内 Hg(II)的滞留时间延长。最后,merH 缺失突变体中 mer 操纵子诱导率降低表明,对 MerH 的需求可能是由于金属向 MerR 转录因子的运输所致。

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