The mntH gene encodes the major Mn(2+) transporter in Bradyrhizobium japonicum and is regulated by manganese via the Fur protein.
The mntH gene encodes the major Mn(2+) transporter in Bradyrhizobium japonicum and is regulated by manganese via the Fur protein.
复制标题
DOI：
10.1111/j.1365-2958.2009.06650.x
复制
发表时间：
2009-04
影响因子：
3.6
通讯作者：
O'Brian MR
中科院分区：
文献类型：
--
作者：
Hohle TH;O'Brian MR
细菌Nramp家族蛋白MntH是二价金属转运蛋白，但mntH突变体在已研究的生物体中几乎没有或没有表型。在这里，我们确定了慢生根瘤菌的mntH同源物，并证明它是必不可少的Mn2+运输和维持细胞锰稳态。在锰缺乏的诱导下，运输活动和Fe 2+不竞争54 Mn 2+的细胞摄取。稳态水平的mntH mRNA的负调控锰，但不受铁。锰的mntH表达和Mn2+运输的控制在毛皮菌株中丢失，导致组成性高活性。在DNA酶I足迹分析中，毛发保护了mntH启动子的35 bp区域，该区域包括完全占用所需的三个不完美的直接重复六聚体。Mn2+使Fur对mntH启动子的亲和力增加了50倍以上，在金属存在下的Kd值为2.2 nM。结果表明MntH是B中主要的Mn 2+转运蛋白。并表明Fur是生物体中锰响应调节剂。此外，Fe 2+既不是MntH的底物，也不是体内mntH表达的调节剂。
The bacterial Nramp family protein MntH is a divalent metal transporter, but mntH mutants have little or no phenotype in organisms where it has been studied. Here, we identify the mntH homolog of Bradyrhizobium japonicum, and demonstrate that it is essential for Mn2+ transport and for maintenance of cellular manganese homeostasis. Transport activity was induced under manganese deficiency, and Fe2+ did not compete with 54Mn2+ for uptake by cells. The steady state level of mntH mRNA was negatively regulated by manganese, but was unaffected by iron. Control of mntH expression and Mn2+ transport by manganese was lost in a fur strain, resulting in constitutively high activity. Fur protected a 35 bp region of the mntH promoter in DNase I footprinting analysis that includes three imperfect direct repeat hexamers that are needed for full occupancy. Mn2+ increased the affinity of Fur for the mntH promoter by over 50-fold, with a Kd value of 2.2 nM in the presence of metal. The findings identify MntH as the major Mn2+ transporter in B. japonicum, and show that Fur is a manganese-responsive regulator in that organism. Furthermore, Fe2+ is neither a substrate for MntH nor a regulator of mntH expression in vivo.
登录
查看更多内容
影响因子：
3.6
作者：
Makui, H;Roig, E;Cellier, MFM
通讯作者：
Cellier, MFM
影响因子：
3.2
作者：
Patzer, SI;Hantke, K
通讯作者：
Hantke, K
影响因子：
3.2
作者：
Kehres, DG;Janakiraman, A;Maguire, ME
通讯作者：
Maguire, ME
影响因子：
2.8
作者：
Díaz-Mireles, E;Wexler, M;Johnston, AWB
通讯作者：
Johnston, AWB
影响因子：
4.8
作者：
Friedman, YE;O'Brian, MR
通讯作者：
O'Brian, MR