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首页> 外文期刊>Microbial Cell Factories >Escherichia coli avoids high dissolved oxygen stress by activation of SoxRS and manganese-superoxide dismutase
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Escherichia coli avoids high dissolved oxygen stress by activation of SoxRS and manganese-superoxide dismutase

机译:大肠杆菌通过激活SoxRS和锰超氧化物歧化酶避免了高溶解氧胁迫

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Background High concentrations of reactive oxygen species (ROS) were reported to cause oxidative stress to E. coli cells associated with reduced or inhibited growth. The high ROS concentrations described in these reports were generated by exposing the bacteria to H2O2 and superoxide-generating chemicals which are non-physiological growth conditions. However, the effect of molecular oxygen on oxidative stress response has not been evaluated. Since the use of oxygen-enriched air is a common strategy to support high density growth of E. coli, it was important to investigate the effect of high dissolved oxygen concentrations on the physiology and growth of E. coli and the way it responds to oxidative stress. Results To determine the effect of elevated oxygen concentrations on the growth characteristics, specific gene expression and enzyme activity in E. coli, the parental and SOD-deficient strain were evaluated when the dissolved oxygen (dO2) level was increased from 30% to 300%. No significant differences in the growth parameters were observed in the parental strain except for a temporary decrease of the respiration and acetate accumulation profile. By performing transcriptional analysis, it was determined that the parental strain responded to the oxidative stress by activating the SoxRS regulon. However, following the dO2 switch, the SOD-deficient strain activated both the SoxRS and OxyR regulons but it was unable to resume its initial growth rate. Conclusion The transcriptional analysis and enzyme activity results indicated that when E. coli is exposed to dO2 shift, the superoxide stress regulator SoxRS is activated and causes the stimulation of the superoxide dismutase system. This enables the E. coli to protect itself from the poisoning effects of oxygen. The OxyR protecting system was not activated, indicating that H2O2 did not increase to stressing levels.
机译:背景技术据报道,高浓度的活性氧(ROS)会导致与减少或抑制生长相关的大肠杆菌细胞氧化应激。这些报告中所述的高ROS浓度是通过将细菌暴露于非生理生长条件的H 2 O 2 和产生超氧化物的化学物质而产生的。但是,尚未评估分子氧对氧化应激反应的影响。由于使用富氧空气是支持大肠杆菌高密度生长的常见策略,因此研究高溶解氧浓度对大肠杆菌的生理和生长及其对氧化反应的反应方式的影响非常重要。强调。结果为确定升高的氧浓度对大肠杆菌的生长特性,特定基因表达和酶活性的影响,在溶解氧(dO 2 )水平下评估了亲本和SOD缺陷菌株。从30%增加到300%。在亲本菌株中,除了呼吸和乙酸盐积累曲线的暂时下降外,在生长参数上没有观察到显着差异。通过进行转录分析,确定亲本菌株通过激活SoxRS调节子对氧化应激作出反应。然而,在dO 2 转换后,SOD缺陷菌株激活了SoxRS和OxyR调节子,但无法恢复其初始生长速度。结论转录分析和酶活性结果表明,当大肠杆菌暴露于dO 2 转变时,超氧化物胁迫调节因子SoxRS被激活并刺激了超氧化物歧化酶系统。这使大肠杆菌能够保护自己免受氧气中毒的影响。 OxyR保护系统未激活,表明H 2 O 2 并未增加至胁迫水平。

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