首页> 外文期刊>Molecular Microbiology >A two-component signal transduction system involved in nickel sensing in the cyanobacterium Synechocystis sp. PCC 6803.
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A two-component signal transduction system involved in nickel sensing in the cyanobacterium Synechocystis sp. PCC 6803.

机译:蓝藻蓝藻属细菌中涉及镍感测的两组分信号转导系统。 PCC 6803。

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摘要

In the cyanobacterium Synechocystis sp. PCC 6803, genes for Ni2+, Co2+, and Zn2+ resistance are grouped in a 12 kb gene cluster. The nrsBACD operon is composed of four genes, which encode proteins involved in Ni2+ resistance. Upstream from nrsBACD, and in opposite orientation, a transcription unit formed by the two genes rppA and rppB has been reported previously to encode a two-component signal transduction system involved in redox sensing. In this report, we demonstrate that rppA and rppB (here redesigned nrsR and nrsS respectively) control the Ni2+-dependent induction of the nrsBACD operon and are involved in Ni2+ sensing. Thus, expression of the nrsBACD operon was not induced by Ni2+ in a nrsRS mutant strain. Furthermore, nrsRS mutant cells showed reduced tolerance to Ni2+. Whereas the nrsBACD operon is transcribed from two different promoters, one constitutive and the other dependent on the presence of Ni2+ in the medium, the nrsRS operon is transcribed from a single Ni2+-inducible promoter. The nrsRS promoter is silent in a nrsRS mutant background suggesting that the system is autoregulated. Purified full length NrsR protein is unable to bind to the nrsBACD-nrsRS intergenic region; however, an amino-terminal truncated protein that contains the DNA binding domain of NrsR binds specifically to this region. Our nrsRS mutant, which carries a deletion of most of the nrsR gene and part of the nrsS gene, does not show redox imbalance or photosynthetic gene mis-expression, contrasting with the previously reported nrsR mutant.
机译:在蓝藻中,Synechocystis sp.。 PCC 6803,Ni2 +,Co2 +和Zn2 +抗性的基因分组在一个12 kb的基因簇中。 nrsBACD操纵子由四个基因组成,编码与Ni2 +抗性有关的蛋白质。在nrsBACD的上游,并且方向相反,先前已经报道了由两个基因rppA和rppB形成的转录单位编码了涉及氧化还原感测的两组分信号转导系统。在本报告中,我们证明了rppA和rppB(分别在此处重新设计了nrsR和nrsS)控制nrsBACD操纵子的Ni2 +依赖性诱导,并参与Ni2 +感测。因此,在nrsRS突变株中,Ni2 +不会诱导nrsBACD操纵子的表达。此外,nrsRS突变细胞显示出对Ni2 +的耐受性降低。尽管从两个不同的启动子转录nrsBACD操纵子,一个是组成型,另一个则取决于培养基中Ni2 +的存在,而从单个Ni2 +诱导型启动子转录nrsRS操纵子。 nrsRS启动子在nrsRS突变体背景下沉默,表明系统是自动调节的。纯化的全长NrsR蛋白无法结合到nrsBACD-nrsRS基因间区域;但是,包含NrsR的DNA结合结构域的氨基末端截短蛋白会与此区域特异性结合。与先前报道的nrsR突变体相比,我们的nrsRS突变体带有大部分nrsR基因和部分nrsS基因的缺失,没有显示氧化还原失衡或光合基因表达错误。

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