The right answer is 3. the availability of tryptophan in the environment
The TRP operon regulation depends on the availability of the tryptophan molecule (it depends if the cell need tryptophan or already has it).
There are two modes of regulation of the trp operon: Suppression and Mitigation
*Repression
The synthesis of operon mRNA is controlled by a repressor that blocks transcription when bound by tryptophan, which acts as a co-repressor.
The repressor, a 108 aa homodimer (ie 2 apo-repressor), has helix-turn-helix domains that interact with inverted repeats at the major groove of the operator, thus allowing its fixation.
In the absence of trp, the repressor is inactive and does not attach to the operator. The RNA polymerase can bind to the promoter and transcribe the trp E, D, C, B, A structural genes.
In the presence of trp, the repressor changes conformation and becomes active, so it binds to the operator, preventing RNA polymerase from accessing the promoter so transcription will not occur.
* The Attenuation
This is a premature termination of transcription that is a function of Trp concentration. It takes place at a late moment of transcription while regulation by repression is done during the initiation.
1st Case: Low Trp Rate, Continuous Transcription, → Formation of the Anti-attenuator in the absence of trp, and therefore the synthesis of tryptophan is continued.
2nd case: High rate of trp, stop transcription, → Formation of the attenuator in the presence of trp. This one will attenuate the synthesis of tryptophan.
