The SoxRS response of Escherichia coli is directly activated by redox-cycling drugs rather than by superoxide.
The SoxRS response of Escherichia coli is directly activated by redox-cycling drugs rather than by superoxide.
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DOI：
10.1111/j.1365-2958.2010.07520.x
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发表时间：
2011-03
影响因子：
3.6
通讯作者：
Imlay JA
中科院分区：
文献类型：
--
作者：
Gu M;Imlay JA
当大肠杆菌暴露于氧化还原循环药物时，其SoxR转录因子被其[2Fe-2S]簇氧化激活。在有氧细胞中，这些药物产生超氧化物，并且由于超氧化物歧化酶（SOD）是SoxRS调控的一员，超氧化物最初被认为是SoxR的激活剂。因此，它的多基因调控被认为包含对超氧化物应激的防御。然而，我们发现大量的超氧化物不能有效激活SOD突变体中的SoxR，过量产生的SOD不能抑制氧化还原循环药物的激活，并且氧化还原循环药物能够激活厌氧细胞中的SoxR，只要提供替代呼吸受体。因此，超氧化物不是SoxR感知到的信号。事实上，在体外，氧化还原循环药物直接氧化纯化的SoxR簇，而超氧化物则没有。氧化还原循环药物由细菌和植物排出。它们的毒性不需要超氧化物，因为它们在厌氧条件下中毒大肠杆菌，部分是通过氧化脱水酶铁硫簇。在这些条件下，SoxRS诱导具有保护作用。因此，从生理上讲，SoxR蛋白直接感知氧化还原循环药物而不是超氧化物是合适的。
When Escherichia coli is exposed to redox-cycling drugs, its SoxR transcription factor is activated by oxidation of its [2Fe–2S] cluster. In aerobic cells these drugs generate superoxide, and because superoxide dismutase (SOD) is a member of the SoxRS regulon, superoxide was initially thought to be the activator of SoxR. Its many-gene regulon was therefore believed to comprise a defense against superoxide stress. However, we found that abundant superoxide did not effectively activate SoxR in an SOD− mutant, that overproduced SOD could not suppress activation by redox-cycling drugs, and that redox-cycling drugs were able to activate SoxR in anaerobic cells as long as alternative respiratory acceptors were provided. Thus superoxide is not the signal that SoxR senses. Indeed, redox-cycling drugs directly oxidized the cluster of purified SoxR in vitro, while superoxide did not. Redox-cycling drugs are excreted by both bacteria and plants. Their toxicity does not require superoxide, as they poisoned E. coli under anaerobic conditions, in part by oxidizing dehydratase iron-sulfur clusters. Under these conditions SoxRS induction was protective. Thus it is physiologically appropriate that the SoxR protein directly senses redox-cycling drugs rather than superoxide.
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影响因子：
3.6
作者：
Anjem A;Varghese S;Imlay JA
通讯作者：
Imlay JA
DOI：
10.1073/pnas.151243198
发表时间：
2001-07-03
影响因子：
11.1
作者：
Gralnick, J;Downs, D
通讯作者：
Downs, D
影响因子：
3.2
作者：
COMPAN, I;TOUATI, D
通讯作者：
TOUATI, D
影响因子：
3.6
作者：
Dietrich, Lars E. P.;Price-Whelan, Alexa;Newman, Dianne K.
通讯作者：
Newman, Dianne K.
DOI：
10.1073/pnas.120163297
发表时间：
2000-06-06
影响因子：
11.1
作者：
Datsenko, KA;Wanner, BL
通讯作者：
Wanner, BL