摘要The SOS (save our soul) response induced by DNA damage in bacteria E coli has raised a great interests in biophysics and has been extensively studied. Previously we have developed a stochastic simulation model to explain the oscillatory-like modulation of SOS gene expression observed in experiment. Here we present an improved semi-stochastic model which has higher simulation efficiency, taking into account the updated knowledge about SOS response. The improved model suggests that frequency of the modulation is controlled by the negative feedback in the system. DNA polymerase V, the key enzyme for error-prone translesion synthesis during SOS response, plays a major role in closing up the negative feedback. It is also indicated that the correlation between the modulation and cellular growth observed in experiment is due to DNA damage induced slowing down of transcription and translation.
Abstract:The SOS (save our soul) response induced by DNA damage in bacteria E coli has raised a great interests in biophysics and has been extensively studied. Previously we have developed a stochastic simulation model to explain the oscillatory-like modulation of SOS gene expression observed in experiment. Here we present an improved semi-stochastic model which has higher simulation efficiency, taking into account the updated knowledge about SOS response. The improved model suggests that frequency of the modulation is controlled by the negative feedback in the system. DNA polymerase V, the key enzyme for error-prone translesion synthesis during SOS response, plays a major role in closing up the negative feedback. It is also indicated that the correlation between the modulation and cellular growth observed in experiment is due to DNA damage induced slowing down of transcription and translation.
NI Ming;WANG Si-Yuan;OUYANG Qi. Modelling the SOS Response by Semi-Stochastic Simulation[J]. 中国物理快报, 2008, 25(7): 2702-2705.
NI Ming, WANG Si-Yuan, OUYANG Qi. Modelling the SOS Response by Semi-Stochastic Simulation. Chin. Phys. Lett., 2008, 25(7): 2702-2705.