Integrated stress response of Escherichia coli to methylglyoxal: transcriptional readthrough from the nemRA operon enhances protection through increased expression of glyoxalase I.
Integrated stress response of Escherichia coli to methylglyoxal: transcriptional readthrough from the nemRA operon enhances protection through increased expression of glyoxalase I.
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DOI：
10.1111/mmi.12234
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发表时间：
2013-06
影响因子：
3.6
通讯作者：
Booth IR
中科院分区：
文献类型：
--
作者：
Ozyamak E;de Almeida C;de Moura AP;Miller S;Booth IR
甲基乙二醛（MG）可增强K+外排系统的激活，以保护细胞免受亲电试剂的毒性。ChIP芯片靶向RNA聚合酶，由一系列其他生物化学测量和突变体创建支持，用于识别响应MG转录的基因，并补充这种快速反应。SOS DNA修复调节子在MG的细胞毒性水平下被诱导，即使暴露于MG是短暂的。MG核心保护系统中，单独的乙二醛酶I是针对MG暴露而诱导的。增加的表达是诱导上游nemRA操纵子的间接结果，编码本身不有助于MG解毒的酶系统。此外，通过nemRA的这种诱导仅在细胞暴露于生长抑制浓度的MG时发生。我们表明，kdpFABCDE基因的诱导，这种表达发生作为细胞质K+的耗竭后，随后激活的KefGB K+外排系统。最后，我们的分析表明，响应MG的转录变化是对DNA和蛋白质损伤的高潮，但是一些整合了特定功能，如DNA修复，以增强主要保护系统KefGB的变构激活。
Methylglyoxal (MG) elicits activation of K+ efflux systems to protect cells against the toxicity of the electrophile. ChIP-chip targeting RNA polymerase, supported by a range of other biochemical measurements and mutant creation, was used to identify genes transcribed in response to MG and which complement this rapid response. The SOS DNA repair regulon is induced at cytotoxic levels of MG, even when exposure to MG is transient. Glyoxalase I alone among the core MG protective systems is induced in response to MG exposure. Increased expression is an indirect consequence of induction of the upstream nemRA operon, encoding an enzyme system that itself does not contribute to MG detoxification. Moreover, this induction, via nemRA only occurs when cells are exposed to growth inhibitory concentrations of MG. We show that the kdpFABCDE genes are induced and that this expression occurs as a result of depletion of cytoplasmic K+ consequent upon activation of the KefGB K+ efflux system. Finally, our analysis suggests that the transcriptional changes in response to MG are a culmination of the damage to DNA and proteins, but that some integrate specific functions, such as DNA repair, to augment the allosteric activation of the main protective system, KefGB.
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影响因子：
6
作者：
Aldini, G;Facino, RM;Carini, M
通讯作者：
Carini, M
影响因子：
3.2
作者：
Ferguson, GP;Booth, IR
通讯作者：
Booth, IR
影响因子：
3.6
作者：
FERGUSON, GP;MCLAGGAN, D;BOOTH, IR
通讯作者：
BOOTH, IR
DOI：
10.1073/pnas.0703709104
发表时间：
2007-08-14
影响因子：
11.1
作者：
Fujisawa, Makoto;Ito, Masahiro;Krulwich, Terry A.
通讯作者：
Krulwich, Terry A.
影响因子：
3.2
作者：
EPSTEIN, W;KIM, BS
通讯作者：
KIM, BS