MntR(Rv2788): a transcriptional regulator that controls manganese homeostasis in Mycobacterium tuberculosis.
MntR(Rv2788): a transcriptional regulator that controls manganese homeostasis in Mycobacterium tuberculosis.
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DOI：
10.1111/mmi.13207
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发表时间：
2015-12
影响因子：
3.6
通讯作者：
Rodriguez GM
中科院分区：
文献类型：
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作者：
Pandey R;Russo R;Ghanny S;Huang X;Helmann J;Rodriguez GM
致病性结核分枝杆菌编码金属调节剂 DtxR/MntR 家族的两个成员：IdeR 和 SirR。 IdeR 响应二价铁而抑制基因表达，我们在此证明 SirR (Rv2788) 虽然也被注释为铁依赖性阻遏蛋白，但其功能却作为锰依赖性转录阻遏蛋白，因此被重命名为 MntR。 MntR 调节促进锰输入的转运蛋白和对金属离子缺乏做出反应的基因，例如 esx3 系统。 MntR 对锰输入的抑制对于结核分枝杆菌在高锰可用性条件下的生存至关重要，但在感染过程中 mntR 是可有可无的。相反，发现MntH和MntABCD输入的锰对于结核分枝杆菌在巨噬细胞中的复制是不可或缺的。这些结果表明，锰在宿主体内受到限制，干扰这种必需金属的输入可能是减少结核分枝杆菌的有效策略。
The pathogenic mycobacterium Mycobacterium tuberculosis encodes two members of the DtxR/MntR family of metalloregulators, IdeR and SirR. IdeR represses gene expression in response to ferrous iron, and we here demonstrate that SirR (Rv2788), although also annotated as an iron-dependent repressor, functions instead as a manganese dependent transcriptional repressor and is therefore renamed MntR. MntR regulates transporters that promote manganese import and genes that respond to metal ion deficiency such as the esx3 system. Repression of manganese import by MntR is essential for survival of M. tuberculosis under conditions of high manganese availability, but mntR is dispensable during infection. In contrast, manganese import by MntH and MntABCD was found to be indispensable for replication of M. tuberculosis in macrophages. These results suggest that manganese is limiting in the host and that interfering with import of this essential metal may be an effective strategy to attenuate M. tuberculosis.