Ni Ming, Yang Le, Liu Xi-Li, Qi Ouyang
Center for Theoretical Biology, School of Physics, Peking University, Beijing 100871, People's Republic of China.
Curr Microbiol. 2008 Dec;57(6):521-6. doi: 10.1007/s00284-008-9235-4. Epub 2008 Sep 10.
Bacteria in nature often suffer sudden stresses, such as ultraviolet (UV) irradiation, nutrient deprivation, and chemotoxins that would cause DNA damage and DNA replication failure, which in turn trigger SOS response. According to the strength and duration of the stress, the SOS system not only repairs DNA damage but also induces mutagenesis, so as to adapt to the changing environment. The key proteins in charge of mutagenesis are UmuD and UmuD'. In this paper, we quantitatively measure the growth rate and cellular levels of proteins UmuD and UmuD' in Escherichia coli after various fluences of UV irradiation. To compare with the experimental observations, an ordinary differential equation model is built to describe the SOS response. Considering the fact that the DNA lesions affect cellular protein production and replication origination, the simulation results fit well with the experimental data. Our results show how the fluence of UV irradiation determines the dynamics of the inducing signal and the mutation frequency of the cell.
自然界中的细菌经常遭受突然的压力,如紫外线(UV)照射、营养剥夺和化学毒素,这些会导致DNA损伤和DNA复制失败,进而触发SOS反应。根据压力的强度和持续时间,SOS系统不仅能修复DNA损伤,还会诱导诱变,以适应不断变化的环境。负责诱变的关键蛋白是UmuD和UmuD'。在本文中,我们定量测量了不同紫外线照射通量后大肠杆菌中蛋白UmuD和UmuD'的生长速率和细胞水平。为了与实验观察结果进行比较,建立了一个常微分方程模型来描述SOS反应。考虑到DNA损伤会影响细胞蛋白质产生和复制起始这一事实,模拟结果与实验数据拟合良好。我们的结果表明紫外线照射通量如何决定诱导信号的动态变化以及细胞的突变频率。