Enzyme regulation — ATCase example: The ability of CTP (cytidine triphosphate) to bind allosterically to aspartate carbamoyltransferase (ATCase) and suppress further CTP synthesis is an example of which control mechanism?

Introduction / Context:
Cells economize resources by adjusting pathway flux according to end-product levels. ATCase, a classic regulatory enzyme in pyrimidine biosynthesis, is inhibited by CTP, the pathway's end product. This textbook case illustrates feedback inhibition via allosteric regulation.

Given Data / Assumptions:

• CTP is the end product of the pyrimidine biosynthetic pathway initiated by ATCase.
• CTP binds at a regulatory (allosteric) site, distinct from the active site.
• Binding decreases catalytic activity without changing enzyme amount.

Concept / Approach:
Feedback inhibition occurs when a pathway product inhibits an early, often committed, step to prevent unnecessary synthesis. Allosteric effectors like CTP change the conformation and activity of multimeric enzymes such as ATCase, aligning supply with demand.

Step-by-Step Solution:
Identify the effector: CTP is the end product (feedback signal). Recognize the mechanism: binding at a regulatory site reduces activity. Differentiate activity regulation from gene-level induction/repression. Select “feedback inhibition of enzyme activity.”

Verification / Alternative check:
Kinetic curves of ATCase show shifts upon CTP addition (sigmoidal behavior), consistent with allosteric inhibition, not changes in enzyme expression levels.

Why Other Options Are Wrong:

• Induction / Repression: Refer to gene expression changes, not immediate activity modulation.
• Covalent activation: ATCase regulation here is noncovalent allostery, not phosphorylation.
• None of these: Incorrect because feedback inhibition is precisely what occurs.

Common Pitfalls:
Confusing rapid, reversible allosteric control with slower transcriptional regulation; both exist but act on different timescales.

Final Answer:
Feedback inhibition of enzyme activity (product inhibition via allostery).