Laboratory of Radiation Biology, Joint Institute for Nuclear Research, 6 Joliot-Curie Street, 141980 Dubna, Moscow Region, Russia.
J Theor Biol. 2013 Sep 7;332:30-41. doi: 10.1016/j.jtbi.2013.04.026. Epub 2013 Apr 30.
A theoretical study is performed of the possible role of the methyl-directed mismatch repair system in the ultraviolet-induced mutagenesis of Escherichia coli bacterial cells. For this purpose, mathematical models of the SOS network, translesion synthesis and mismatch repair are developed. Within the proposed models, the key pathways of these repair systems were simulated on the basis of modern experimental data related to their mechanisms. Our model approach shows a possible mechanistic explanation of the hypothesis that the bacterial mismatch repair system is responsible for attenuation of mutation frequency during ultraviolet-induced SOS response via removal of the nucleotides misincorporated by DNA polymerase V (the UmuD'2C complex).
本文针对大肠杆菌细胞中紫外线诱导突变的可能机制,从理论角度研究了甲基导向的错配修复系统的作用。为此,我们构建了 SOS 网络、跨损伤合成和错配修复的数学模型。在所提出的模型中,基于与修复机制相关的现代实验数据,对这些修复系统的关键途径进行了模拟。我们的模型方法为以下假说提供了可能的机制解释,即细菌错配修复系统通过切除 DNA 聚合酶 V(UmuD'2C 复合物)掺入的错误核苷酸来降低紫外线诱导 SOS 反应过程中的突变频率。