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通过比较基因组范围内对铜和锌过量的转录反应分析鉴定沙门氏菌辅助性铜解毒机制。

Identification of a Salmonella ancillary copper detoxification mechanism by a comparative analysis of the genome-wide transcriptional response to copper and zinc excess.

机构信息

Instituto de Biología Molecular y Celular de Rosario, Departamento de Microbiología, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Consejo Nacional de Investigaciones Científicas y Técnicas, Ocampo y Esmeralda, 2000-Rosario, Argentina.

Department of Pathology and Laboratory Medicine, University of California, Irvine, CA, USA.

出版信息

Microbiology (Reading). 2014 Aug;160(Pt 8):1659-1669. doi: 10.1099/mic.0.080473-0. Epub 2014 May 23.

DOI:10.1099/mic.0.080473-0
PMID:24858080
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4117220/
Abstract

Copper and zinc are essential metal ions, but toxic in excess. Bacteria have evolved different strategies to control their intracellular concentrations, ensuring proper supply while avoiding toxicity, including the induction of metal-specific as well as non-specific mechanisms. We compared the transcriptional profiles of Salmonella Typhimurium after exposure to either copper or zinc ions in both rich and minimal media. Besides metal-specific regulatory networks many global stress-response pathways react to an excess of either of these metal ions. Copper excess affects both zinc and iron homeostasis by inducing transcription of these metal-specific regulons. In addition to the control of zinc-specific regulons, zinc excess affects the Cpx regulon and the σ(E) envelope-stress responses. Finally, novel metal-specific upregulated genes were detected including a new copper-detoxification pathway that involves the siderophore enterobactin and the outer-membrane protein TolC. This work sheds light onto the transcriptional landscape of Salmonella after copper or zinc overload, and discloses a new mechanism of copper detoxification.

摘要

铜和锌是必需的金属离子,但过量则有毒。细菌已经进化出不同的策略来控制其细胞内浓度,确保适当的供应,同时避免毒性,包括诱导金属特异性和非特异性机制。我们比较了在丰富和最小培养基中暴露于铜或锌离子后,鼠伤寒沙门氏菌的转录谱。除了金属特异性调节网络外,许多全局应激反应途径对这两种金属离子的过量都有反应。铜过量通过诱导这些金属特异性调控子的转录来影响锌和铁的稳态。除了锌特异性调控子的控制外,锌过量还影响 Cpx 调控子和 σ(E)包膜应激反应。最后,检测到新的金属特异性上调基因,包括涉及铁载体肠杆菌素和外膜蛋白 TolC 的新铜解毒途径。这项工作揭示了沙门氏菌在铜或锌过载后的转录景观,并揭示了一种新的铜解毒机制。

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