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Team:Warsaw/Modelling/Gene Networks
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| + | ===Simplified description of the invasion operon bistable regulation=== | ||
| + | ====Why model?==== | ||
| + | ====Model overview==== | ||
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| + | <img src="https://static.igem.org/mediawiki/2009/1/16/ModelowanieSwitch.jpg"></html> | ||
| + | ====Parameters==== | ||
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| + | ==Simplified description of the cytoplasmatic switch== | ||
| + | This simple model is based on kinetic differential equations which are used to describe the kinetics of chemical reactions. We assumed that all cro proteins is already degraded and only AraC and TetR regulate the expression of the proapoptotic proteins. The abbreviations are the same as the picture that depict the regulatory system. | ||
| + | [[Image:Differential 1.png|thumb|680px|Kinetics of AraC]] | ||
| + | [[Image:Differential 2.png|thumb|680px|Kinetics of Bax]] | ||
| + | The mechanistic consideration are simple. The repressor proteins tightly bind to DNA preventing from initation of transcription. It is assumed that almost all promoters are blocked and one can neglect the cryptic transcription in the model. Addition of tetracycline or arabinose lead to generation of dynamic equlibrium. Some protein molecules create complexes with their ligands which are not blocked the transcription. Due to lack of direct interactions between these two proteins regulation of both transcription is independ. To simplify the equations we also assume that concentration of mRNAs is explicite depend on time and there is no implicit variables in the system. The ratio of translation is equal for all trancripts due to usage the same RBS for all of them. | ||
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Latest revision as of 03:56, 22 October 2009
Contents |
Simplified description of the invasion operon bistable regulation
Why model?
Model overview
Parameters
Simplified description of the cytoplasmatic switch
This simple model is based on kinetic differential equations which are used to describe the kinetics of chemical reactions. We assumed that all cro proteins is already degraded and only AraC and TetR regulate the expression of the proapoptotic proteins. The abbreviations are the same as the picture that depict the regulatory system.
The mechanistic consideration are simple. The repressor proteins tightly bind to DNA preventing from initation of transcription. It is assumed that almost all promoters are blocked and one can neglect the cryptic transcription in the model. Addition of tetracycline or arabinose lead to generation of dynamic equlibrium. Some protein molecules create complexes with their ligands which are not blocked the transcription. Due to lack of direct interactions between these two proteins regulation of both transcription is independ. To simplify the equations we also assume that concentration of mRNAs is explicite depend on time and there is no implicit variables in the system. The ratio of translation is equal for all trancripts due to usage the same RBS for all of them.
