Our goal was to model the concentration of RecA and LexA over time for to gain an understanding of the interaction between the two key players in the SOS repair mechanism.
BUILDING THE MODEL
In building the model we asked ourselves the following questions: How much UV exposure causes actual CPD DNA damage? What will this model do that our experiment can't? How many species from the UV-UvrA pathway do we need to accomplish this?
We were going to model the UV-GFP-tagged-UvrA interactions in a single E.coli cell and make assumptions such that modeling a single cell can be the average representation of all the cells.
The state variables would have likely been the following: 1) UV exposure time * intensity, and 2) GFP concentration.
We eventually decided to model LexA and RecA because they controlled the NER mechanism and their expression was crucial for us to understand how RecA responded to LexA and the LexA to RecA. We modeled the relationship based off of the stochastic analysis done by Shimoni Y. et al [1]. We model the SOS system by defining the concentrations of recA mRNA, lexA mRNA, LexA protein, RecA protein, and LexA proteins bound to the promoter regions of RecA and LexA.
Figure 1. What we modeled
Figure 2. Simulation of the concentration of LexA and RecA over time
Figure 3. Our differential equation of the species modeled
[1] Shimoni Y, Altuvia S, Margalit H, Biham O. (2009) Stochastic analysis of the SOS response in Escherichia coli. PLoS One 4(5): e5363. pmid:19424504
