A literature search revealed two models of IPTG-induced expression through the Plac promoter. Both models assume constitutive expression of LacI. Before IPTG is added, a steady-state is reached comprising basal (leaky) expression of GFP.
In the simpler model (2) IPTG competes with free promoter for LacI binding, but does not itself bind to the LacI-promoter complex.
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Under this model, with all other parameters constant, the steady-state concentration of free promoter and hence the steady-state concentration of GFP are independent of the initial concentration of IPTG. (See time evolution of GFP expression assuming different concentrations of IPTG are used for induction, right.)
The pre-steady-state dynamic behaviour of the GFP concentration will differ with different initial concentrations of IPTG (but the steady-state behaviour will not). Hence, accurate data collection during the pre-steady-state phase is crucial for parameter estimation.
More complex model
A more sophisticated model allows for interaction between IPTG and the promoter-LacI complex (3). IPTG can bind to the promoter-LacI complex to form IPTG-LacI and free promoter. This eases the repression by LacI and allows transcription of GFP.
Under this model, the dynamic behaviour (whether or not [GFP] attains a maximum higher than its steady-state value) depends on the relative strengths of the kinetic constants describing the interactions underlying the model. Either way, the steady-state [GFP] will vary as a Hill-function dependent on the initial concentration of IPTG; this characteristic can be used to discriminate between the two models.
ODEs and simulation m-files for further exploration of the properties of these models can, again, be found in the appendices.
>>> Details of equilibria and equations and qualitative discussion of parameter effects >>>