Department of Chemistry, University of Massachusetts, Amherst, Massachusetts 01003, USA.
J Am Chem Soc. 2012 Apr 25;134(16):7081-93. doi: 10.1021/ja300834b. Epub 2012 Apr 11.
RcnR (resistance to cobalt and nickel regulator) is a 40-kDa homotetrameric protein and metalloregulator that controls the transcription of the Co(II) and Ni(II) exporter, RcnAB, by binding to DNA as an apoprotein and releasing DNA in response to specifically binding Co(II) and Ni(II) ions. Using X-ray absorption spectroscopy (XAS) to examine the structure of metals bound and lacZ reporter assays of the transcription of RcnA in response to metal binding, in WT and mutant proteins, the roles of coordination number, ligand selection, and residues in the N-terminus of the protein were examined as determinants in metal ion recognition. The studies show that the cognate metal ions, Co(II) and Ni(II), which bind in (N/O)(5)S six-coordinate sites, are distinguished from non-cognate metal ions (Cu(I) and Zn(II)), which bind only three protein ligands and one anion from the buffer, by coordination number and ligand selection. Using mutations of residues near the N-terminus, the N-terminal amine is shown to be a ligand of the cognate metal ions that is missing in the complexes with non-cognate metal ions. The side chain of His3 is also shown to play an important role in distinguishing metal ions. The imidazole group is shown to be a ligand in the Co(II) RcnR complex, but not in the Zn(II) complex. Further, His3 does not appear to bind to Ni(II), providing a structural basis for the differential regulation of RcnAB by the two cognate ions. The Zn(II) complexes change coordination number in response to the residue in position three. In H3C-RcnR, the Zn(II) complex is five-coordinate, and in H3E-RcnR the Zn(II) ion is bound to six protein ligands. The metric parameters of this unusual Zn(II) structure resemble those of the WT-Ni(II) complex, and the mutant protein is able to regulate expression of RcnAB in response to binding the non-cognate ion. The results are discussed within a protein allosteric model for gene regulation by metalloregulators.
RcnR(钴和镍调节剂抗性)是一种 40kDa 的同源四聚体蛋白和金属调节剂,通过作为无蛋白结合 DNA 并响应特定结合 Co(II)和 Ni(II)离子释放 DNA来控制 Co(II)和 Ni(II)出口器 RcnAB 的转录。使用 X 射线吸收光谱(XAS)检查结合金属的结构以及金属结合时 WT 和突变蛋白中 RcnA 转录的 lacZ 报告基因测定,研究了配位数、配体选择以及蛋白质 N 末端残基在金属离子识别中的作用。研究表明,与非配位金属离子(Cu(I)和 Zn(II))相比,结合(N/O)(5)S 六配位位点的同源金属离子 Co(II)和 Ni(II)通过配位数和配体选择来区分。使用靠近 N 末端的残基突变,表明 N 末端胺是配位金属离子的配体,而在与非配位金属离子的配合物中缺失。还表明 His3 的侧链在区分金属离子方面也起着重要作用。表明咪唑基团是 Co(II)RcnR 配合物中的配体,但不是 Zn(II)配合物中的配体。此外,His3 似乎不与 Ni(II)结合,为两种同源离子对 RcnAB 的差异调节提供了结构基础。Zn(II)配合物响应位置三的残基改变配位数。在 H3C-RcnR 中,Zn(II)配合物是五配位的,而在 H3E-RcnR 中,Zn(II)离子与六个蛋白质配体结合。这种不寻常的 Zn(II)结构的度量参数与 WT-Ni(II)配合物的相似,并且突变蛋白能够响应结合非配位离子来调节 RcnAB 的表达。结果在金属调节剂基因调控的蛋白质变构模型内进行了讨论。