Glucose-dependent TetR expression
CAP promoter regulates expression in dependency of glucose. TetR binds to the pTet regulator inhibiting transcription. Anhydrotetracycline binds to TetR inhibiting its operation.
Usage and Biology
This part originates from the Lactose operon. The operator - binding site of LacI - was deleted to yield a lactose independent regulatory system. It is known that the Lactose operon also responds to catabolite repression, which is now the only regulatory element within the promoter, making it solely dependent on glucose. If the glucose concentration is LOW, the bacterial Adenylate Cyclase is active and synthesises cAMP (cyclic AMP), which interacts with CAP (catabolite activating protein). The CAP-cAMP complex then binds the CAP binding site potentially activating transcription of TetR. This consequently leads to the inactivation of the transcription from the pTet.
If the glucose concentration increases, the Catabolite Repression system will inhibit the expression of TetR and consequently the genes downstream of pTet could be transcribed.
Sequence and Features
- 10COMPATIBLE WITH RFC
- 12COMPATIBLE WITH RFC
- 21COMPATIBLE WITH RFC
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- 25COMPATIBLE WITH RFC
- 1000COMPATIBLE WITH RFC