Imported:YPM/Major assumptions and points of contention
Due to the complexity of the pheromone response pathway, and the uncertainty in our knowledge of its function, many simplifying assumptions were made in order to build the model. Some of these assumptions are rather benign, but others are likely to be somewhat contentious. Below is a list of potentially contentious assumptions or simplifications that have been made, and that could be changed for a more detailed or accurate model.
- Since it does not appear that Ste50/Ste11 binding is modulated at all by pheromone treatment (see Ste11/Ste50 interactions for more details), we will ignore the details of Ste50 binding to Ste11, and assume that the effects of this interaction are taken into account by the rates of reaction involving Ste11.
Tec1 is not included in the model.
- Although Tec1 may not strictly be part of the pheromone response pathway, its dynamics (interactions with Ste12 and Fus3-dependent degradation) would be interesting to model.
- Saturation kinetics for Ste12-mediated gene expression could be replaced with a different relationship (perhaps a Hill function) or with more detailed molecular reactions.
Sst2 binding to Gpa1 in the model occurs via the binding of both molecules to Ste2, not via direct binding between Sst2 and Gpa1. Thus, the Sst2-mediated acceleration of Gpa1's hydrolysis of bound GTP occurs via a catalytic event within a trimeric complex of Sst2, Ste2, and Gpa1.
- See RGS(Sst2)/Galpha(Gpa1)/Receptor(Ste2) interactions for more details.
- See MAPK_phosphorylation_cascade for more details.
Ste12 phosphorylation not required for its activation.
- See Dig1/Dig2/Ste12 phosphorylation for more details.
- This interactions would be most interesting when modeled with cell cycle dependent activation of Cdc28.
Cell cycle effect on pathway response is not modeled.