Which of the following statements is true of the regulation of tryptophan biosynthesis gene expression in bacteria?

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Question: Which of the following statements is true of the regulation of tryptophan biosynthesis gene expression in bacteria?

Option 1: 'Five enzymes related to tryptophan biosynthesis genes are under the control of 5 different promoters' This is not accurate. In the classical trp operon model of E. coli, the regulation centers on a single operon that encodes several enzymes, coordinated by shared regulatory elements, not five separately controlled promoters for each enzyme. The emphasis is on operon-level regulation rather than independent promoters for each enzyme.

Option 2: 'When tryptophan is low but other amino acids are lacking, RNA polymerase binds tightly and does not undergo attenuation' This statement is misleading. Attenuation is a regulatory mechanism that depends on the availability of tryptophan specifically; low tryptophan typically reduces attenuation, allowing transcription to proceed. The claim that RNA polymerase binds tightly and blocks transcription under low tryptophan (and lacking other amino acids) is inconsistent with the classic mechanism, which uses tryptophan levels as the key signal for attenuation.

Option 3: 'In the absence of tryptophan the repressor is bound to the operator' The repressor in the trp operon requires tryptophan as a corepressor to become active and bind the operator. In the absence of tryptophan, the repressor is inactive and cannot bind the operator, allowing transcription to proceed. Thus this statement is false.

Option 4: 'In the presence of high tryptophan, the repressor is bound to the operator' This aligns with the canonical model. Tryptophan acts as a corepressor by binding to the aporepressor, activating it to form the holo-repressor, which then binds to the operator to block transcription of the tryptophan biosynthesis genes. Therefore, transcription is repressed when tryptophan levels are high.

Option 5: 'In the presence of low tryptophan, the repressor is bound to the promoter' This is incorrect for multiple reasons. When tryptophan is low, the repressor is inactive and cannot bind the operator; there is no canonical mechanism in which the repressor binds a promoter to regulate transcription in this context. The promoter is generally accessible for transcription initiation, and attenuation/operon-level control governs expression in response to tryptophan levels, not promoter-bound repression by a repressor in low-tryptophan conditions.

In summary, only the statement describing high tryptophan enabling the repressor to bind the operator accurately reflects the regulatory mechanism of the tryptophan biosynthesis operon in bacteria, where tryptophan acts as a corepressor to inhibit transcription by the repressor-operator interaction. The other options misstate how attenuation works, the role of tryptophan as a corepressor, or the organization of the operon’s regulation.

Which of the following statements is true of the regulation of tryptophan biosynthesis gene expression in bacteria?

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