Magnesium-dependent processes are targets of bacterial manganese toxicity.
Magnesium-dependent processes are targets of bacterial manganese toxicity.
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DOI：
10.1111/mmi.12687
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发表时间：
2014-08
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
编码高亲和力Mn 2+转运蛋白MntH的基因缺陷的慢生根瘤菌突变体在锰限制下具有严重的生长表型。在这里，我们分离的mntH菌株，锰限制下生长的抑制突变体，高亲和力Mn 2+运输和Mn 2+依赖酶的活动被部分救出。抑制菌株在编码Mg 2+通道MgtE的基因中具有功能获得性突变。MgtE变体可能通过门控机制的丧失允许Mn 2+进入，当细胞Mg 2+水平高时，门控机制通常将转运蛋白保持在关闭状态。MgtE依赖性和非依赖性抑制基因表型都被镁限制性生长的mntH菌株所概括。野生型细胞的生长研究表明，当环境镁含量低时，锰对细胞是有毒的。此外，细胞外锰和镁的水平被操纵，以抑制生长，而基本上不改变细胞内的金属含量，这意味着锰的毒性取决于其细胞分布，而不是绝对浓度。Mn ~（2+）对Mg ~（2+）依赖性酶活性有抑制或促进作用。我们的结论是，Mn 2+可以占据Mg 2+结合位点的细胞，并建议镁依赖的过程是锰毒性的目标。
A Bradyrhizobium japonicum mutant defective in the gene encoding the high affinity Mn2+ transporter MntH has a severe growth phenotype under manganese limitation. Here, we isolated suppressor mutants of an mntH strain that grew under manganese limitation, and activities of high affinity Mn2+ transport and Mn2+-dependent enzymes were partially rescued. The suppressor strains harbor gain-of-function mutations in the gene encoding the Mg2+ channel MgtE. The MgtE variants likely allow Mn2+ entry via loss of a gating mechanism that normally holds the transporter in the closed state when cellular Mg2+ levels are high. Both MgtE-dependent and -independent suppressor phenotypes were recapitulated by magnesium-limited growth of the mntH strain. Growth studies of wild type cells suggest that manganese is toxic to cells when environmental magnesium is low. Moreover, extracellular manganese and magnesium levels were manipulated to inhibit growth without substantially altering the intracellular content of either metal, implying that manganese toxicity depends on its cellular distribution rather than the absolute concentration. Mg2+-dependent enzyme activities were found to be inhibited or stimulated by Mn2+. We conclude that Mn2+ can occupy Mg2+-binding sites in cells, and suggest that Mg2+-dependent processes are targets of manganese toxicity.
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影响因子：
3.2
作者：
CHARNEY, J;FISHER, WP;HEGARTY, CP
通讯作者：
HEGARTY, CP
影响因子：
3.6
作者：
Martin JE;Imlay JA
通讯作者：
Imlay JA
影响因子：
3.6
作者：
Hohle TH;O'Brian MR
通讯作者：
O'Brian MR
影响因子：
3.6
作者：
Anjem A;Varghese S;Imlay JA
通讯作者：
Imlay JA
DOI：
10.1073/pnas.1110137108
发表时间：
2011-09-13
影响因子：
11.1
作者：
Hohle, Thomas H.;Franck, William L.;O'Brian, Mark R.
通讯作者：
O'Brian, Mark R.