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Involvement of alkylhydroxybenzenes in the Escherichia coli response to the lethal effect of UV irradiation

机译:烷基羟苯类参与大肠杆菌对紫外线辐射的致死作用的反应

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This work is concerned with the role of alkylhydroxybenzenes (AHBs), chemical analogs of the autoregulatory microbial d _1 factors, on the development of the stress response of bacterial cells to UV irradiation, including SOS system induction, preservation of cell viability, and S → R phase transitions of the Escherichia coli test strain with the bioluminescence genes cloned under the control of the recA gene promoter. UV irradiation, a natural stress factor, and an increase in AHB concentrations were found to elicit uniform responses in bacteria, indicating that AHBs function as alarmones, i. e., alarm signals. It was revealed that preincubating bacteria with alkylhydroxybenzenes considerably enhanced their viability upon irradiation with lethal UV doses; this was accompanied by a relative decrease in the SOS response activity and a concomitant increase in the frequency of phase transitions. The efficiency of the protective action of AHBs increased with an increase in their hydrophobicity degree. The probable mechanism of the protective effect of AHBs is discussed, based on their capacity for the interaction with biopolymers, which results in changing their structural organization and conferring resistance to a broad spectrum of stress factors. Such a "passive" protective mechanism reduces the susceptibility of DNA to UV irradiation, causing a decrease in the parameters related to the SOS system induction that is responsible for the "active" protective mechanism in bacterial cells. As a result, viability retention under the lethal influence of UV irradiation is possible at minimal values of repair activity and is accompanied by an increase in the phenotypic variability of the surviving part of a bacterial population.
机译:这项工作涉及烷基羟基苯(AHBs),自调控微生物d _1因子的化学类似物在细菌细胞对紫外线辐射的应激反应的发展中的作用,包括SOS系统诱导,细胞活力的维持和S→具有在recA基因启动子控制下克隆的生物发光基因的大肠杆菌测试菌株的R相转变。发现紫外线辐射,自然胁迫因素和AHB浓度的增加会引起细菌中的均匀反应,这表明AHBs起到了警报作用,即。例如,警报信号。结果表明,在用致命的紫外线照射后,将细菌与烷基羟基苯预孵育会大大提高其生存能力。这伴随着SOS响应活性的相对下降和相变频率的相应增加。 AHBs的保护作用效率随其疏水度的增加而增加。基于AHBs与生物聚合物相互作用的能力,讨论了AHBs保护作用的可能机制,这导致其结构组织发生变化,并赋予了对多种应力因素的抗性。这种“被动”保护机制降低了DNA对紫外线辐射的敏感性,导致与SOS系统诱导有关的参数降低,而SOS系统诱导是细菌细胞中“主动”保护机制的原因。结果,在最小的修复活性值下,在紫外线辐射的致命影响下的存活力保持是可能的,并且伴随着细菌种群存活部分的表型变异性的增加。

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