Q.89 Control mechanisms operate at any of the several steps involved in gene expression. Which one of
the following is the key mode of regulation during the cell cycle?
(A) Transcription
(B) mRNA processing
(C) Activation of protein function resulting from protein-protein interaction
(D) mRNA export
Cell cycle regulation primarily occurs through activation of protein function via protein-protein interactions, particularly cyclin-CDK complex formation.
The correct answer is (C).
Cell Cycle Control Overview
The cell cycle depends on cyclin-dependent kinases (CDKs) oscillating with cyclins. Inactive apo-CDKs require cyclin binding (protein-protein interaction) for activation, plus CAK phosphorylation. These complexes drive G1/S, S, G2/M transitions via substrate phosphorylation (e.g., Rb → E2F release). Checkpoints monitor via CKIs (p21, p27) binding same complexes.
Option Breakdown
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(A) Transcription: Wrong—cyclin transcription occurs but isn’t “key mode”; protein-level activation times transitions precisely (e.g., cyclin B surge triggers mitosis).
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(B) mRNA processing: Wrong—eukaryotic splicing irrelevant; cyclins lack complex regulation here vs. rapid proteolysis/degradation control.
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(C) Protein-protein interaction activation: Correct—cyclin-CDK binding, CKI inhibition, CAK binding exemplify post-translational control as primary oscillator.
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(D) mRNA export: Wrong—nuclear export minor; cyclin levels controlled by synthesis/degradation, not export bottlenecks.
Introduction to Cell Cycle Regulation Protein Protein Interaction
Cell cycle regulation protein protein interaction via cyclin-CDK complexes drives ordered progression—core GATE Life Sciences topic. Cyclin binding activates CDKs for Rb phosphorylation, DNA licensing; far surpasses transcriptional control in immediacy.
CDK Activation Cascade
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G1: Cyclin D-CDK4/6 → Rb hyperphosphorylation → S-phase entry.
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S: Cyclin E/A-CDK2 → DNA replication origins fire.
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M: Cyclin B-CDK1 → chromosome condensation, spindle assembly.
CKIs (p21/p27) bind complexes to halt at checkpoints (DNA damage, incomplete replication).
Why Not Other Levels?
| Option | Role | Why Not Key? |
|---|---|---|
| (A) Transcription | Cyclin synthesis | Too slow for transitions |
| (B) Processing | Rare regulation | Cyclins lack introns typically |
| (C) Protein interaction | CDK activation | Precise, rapid timing |
| (D) Export | Minor nuclear-cyclin traffic | Degradation dominates |
GATE Strategy
Cell cycle regulation protein protein interaction = cyclin-CDK hallmark. Distinguish post-translational (C) from transcriptional (A). Master: “No cyclin, no division.” PYQ answer: (C).
