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紫外线B照射下具有缺陷修复机制的大肠杆菌细胞中的存活及SOS反应诱导

Survival and SOS response induction in ultraviolet B irradiated Escherichia coli cells with defective repair mechanisms.

作者信息

Prada Medina Cesar Augusto, Aristizabal Tessmer Elke Tatjana, Quintero Ruiz Nathalia, Serment-Guerrero Jorge, Fuentes Jorge Luis

机构信息

a Laboratorio de Microbiología y Mutagénesis Ambiental, Grupo de Investigaciòn en Microbiología y Genética, Escuela de Biología , Universidad Industrial de Santander , Bucaramanga , Colombia ;

b Departamento de Biología , Instituto Nacional de Investigaciones Nucleares , Distrito Federal , México.

出版信息

Int J Radiat Biol. 2016 Jun;92(6):321-8. doi: 10.3109/09553002.2016.1152412. Epub 2016 Mar 11.

Abstract

Purpose In this paper, the contribution of different genes involved in DNA repair for both survival and SOS induction in Escherichia coli mutants exposed to ultraviolet B radiation (UVB, [wavelength range 280-315 nm]) was evaluated. Materials and methods E. coli strains defective in uvrA, oxyR, recO, recN, recJ, exoX, recB, recD or xonA genes were used to determine cell survival. All strains also had the genetic sulA::lacZ fusion, which allowed for the quantification of SOS induction through the SOS Chromotest. Results Five gene products were particularly important for survival, as follows: UvrA > RecB > RecO > RecJ > XonA. Strains defective in uvrA and recJ genes showed elevated SOS induction compared with the wild type, which remained stable for up to 240 min after UVB-irradiation. In addition, E. coli strains carrying the recO or recN mutation showed no SOS induction. Conclusions The nucleotide excision and DNA recombination pathways were equally used to repair UVB-induced DNA damage in E. coli cells. The sulA gene was not turned off in strains defective in UvrA and RecJ. RecO protein was essential for processing DNA damage prior to SOS induction. In this study, the roles of DNA repair proteins and their contributions to the mechanisms that induce SOS genes in E. coli are proposed.

摘要

目的 在本文中,评估了参与DNA修复的不同基因对暴露于紫外线B辐射(UVB,[波长范围280 - 315nm])的大肠杆菌突变体的存活和SOS诱导的贡献。材料和方法 使用在uvrA、oxyR、recO、recN、recJ、exoX、recB、recD或xonA基因中有缺陷的大肠杆菌菌株来确定细胞存活率。所有菌株还具有遗传sulA::lacZ融合,这允许通过SOS色测试对SOS诱导进行定量。结果 有五种基因产物对存活特别重要,如下:UvrA>RecB>RecO>RecJ>XonA。与野生型相比,uvrA和recJ基因有缺陷的菌株显示出更高的SOS诱导,在UVB照射后长达240分钟内保持稳定。此外,携带recO或recN突变的大肠杆菌菌株未显示出SOS诱导。结论 核苷酸切除和DNA重组途径同等地用于修复大肠杆菌细胞中UVB诱导的DNA损伤。在uvrA和RecJ有缺陷的菌株中,sulA基因未关闭。RecO蛋白对于在SOS诱导之前处理DNA损伤至关重要。在本研究中,提出了DNA修复蛋白的作用及其对大肠杆菌中诱导SOS基因机制的贡献。

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