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不断变化的环境中大肠杆菌的铜稳态机制。

Escherichia coli mechanisms of copper homeostasis in a changing environment.

作者信息

Rensing Christopher, Grass Gregor

机构信息

Department of Soil, Water, and Environmental Science, University of Arizona, Shantz Bld. #38, Rm. 429, Tucson, AZ 85721, USA.

出版信息

FEMS Microbiol Rev. 2003 Jun;27(2-3):197-213. doi: 10.1016/S0168-6445(03)00049-4.

Abstract

Escherichia coli is equipped with multiple systems to ensure safe copper handling under varying environmental conditions. The Cu(I)-translocating P-type ATPase CopA, the central component in copper homeostasis, is responsible for removing excess Cu(I) from the cytoplasm. The multi-copper oxidase CueO and the multi-component copper transport system CusCFBA appear to safeguard the periplasmic space from copper-induced toxicity. Some strains of E. coli can survive in copper-rich environments that would normally overwhelm the chromosomally encoded copper homeostatic systems. Such strains possess additional plasmid-encoded genes that confer copper resistance. The pco determinant encodes genes that detoxify copper in the periplasm, although the mechanism is still unknown. Genes involved in copper homeostasis are regulated by MerR-like activators responsive to cytoplasmic Cu(I) or two-component systems sensing periplasmic Cu(I). Pathways of copper uptake and intracellular copper handling are still not identified in E. coli.

摘要

大肠杆菌配备了多种系统,以确保在不同环境条件下安全处理铜。铜(I)转运P型ATP酶CopA是铜稳态的核心组成部分,负责从细胞质中去除过量的铜(I)。多铜氧化酶CueO和多组分铜转运系统CusCFBA似乎能保护周质空间免受铜诱导的毒性。一些大肠杆菌菌株能够在富含铜的环境中存活,而这种环境通常会使染色体编码的铜稳态系统不堪重负。此类菌株拥有额外的质粒编码基因,赋予其铜抗性。pco决定簇编码在周质中使铜解毒的基因,尽管其机制尚不清楚。参与铜稳态的基因由响应细胞质铜(I)的MerR样激活剂或感知周质铜(I)的双组分系统调控。大肠杆菌中铜的摄取途径和细胞内铜的处理方式仍未明确。

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