Catabolite repression scenario: In the presence of glucose, which regulatory event occurs at the lac promoter region?

Introduction / Context:
Glucose availability affects the lac operon by modulating cAMP levels and CAP binding, a process called catabolite repression. This ensures E. coli preferentially uses glucose before lactose.

Given Data / Assumptions:

• High glucose → low adenylate cyclase activity → low cAMP.
• Low cAMP → less CAP–cAMP complex bound at the promoter.
• Lac repressor responds to lactose/allolactose, not directly to glucose.

Concept / Approach:
Transcription of lac genes requires both repressor relief (induction by lactose/allolactose) and CAP activation (high cAMP). Glucose specifically depresses cAMP, weakening CAP activation.

Step-by-Step Solution:
Relate glucose to cAMP: glucose present → cAMP decreases. Relate cAMP to CAP binding: low cAMP → less CAP–DNA binding. Choose the option describing decreased CAP–cAMP binding.

Verification / Alternative check:
Classic diauxic growth curves show lag in lactose utilization until glucose is depleted, reflecting CAP–cAMP control.

Why Other Options Are Wrong:
Glucose does not increase cAMP; glucose alone does not upregulate lacZ; LacI does not automatically dissociate due to glucose.

Common Pitfalls:
Confusing repressor induction with catabolite repression; assuming glucose directly affects LacI binding.

Final Answer:
Binding of CAP–cAMP complex to the promoter area decreases markedly.