Cell cycle regulation MCQs With Answer

Introduction: This question set on Cell Cycle Regulation is tailored for M.Pharm students studying Cellular and Molecular Pharmacology. It focuses on molecular mechanisms controlling progression through G1, S, G2 and M phases, the key regulators (cyclins, CDKs, CDK inhibitors, checkpoint kinases, APC/C and SCF ubiquitin ligases), and the DNA damage response pathways that govern cell-cycle checkpoints. Clinical relevance is emphasized by including pharmacological modulators such as microtubule-targeting agents and CDK4/6 inhibitors, and how disruption of these pathways contributes to cancer. These MCQs aim to deepen conceptual understanding and to help prepare for exams and drug-development applications involving cell-cycle targets.

Q1. What is the primary biochemical function of cyclin–CDK complexes in cell-cycle control?

• They phosphorylate specific substrate proteins to drive phase transitions
• They directly ubiquitinate proteins to promote degradation
• They form structural components of the mitotic spindle
• They act as membrane receptors for growth factors

Correct Answer: They phosphorylate specific substrate proteins to drive phase transitions

Q2. The G1/S checkpoint primarily monitors which cellular conditions before DNA replication is initiated?

• DNA integrity and mitotic spindle attachment
• Nutrient status and completion of cytokinesis
• DNA damage and growth factor signaling
• Chromosome segregation and cohesin cleavage

Correct Answer: DNA damage and growth factor signaling

Q3. How does p53 typically induce G1 arrest following DNA damage?

• By acting as a kinase that phosphorylates CDKs
• By transcriptionally activating p21 which inhibits cyclin–CDK activity
• By promoting proteasomal degradation of Rb
• By directly binding DNA replication origins to block firing

Correct Answer: By transcriptionally activating p21 which inhibits cyclin–CDK activity

Q4. What is the principal function of the retinoblastoma protein (Rb) in G1 phase?

• To phosphorylate E2F transcription factors
• To bind and inhibit E2F, preventing S-phase gene transcription
• To ubiquitinate cyclin D for degradation
• To activate the anaphase-promoting complex

Correct Answer: To bind and inhibit E2F, preventing S-phase gene transcription

Q5. The anaphase-promoting complex or cyclosome (APC/C) is best described as which type of regulator?

• A serine/threonine phosphatase activating CDKs
• An E3 ubiquitin ligase that targets securin and cyclin B for degradation
• A DNA helicase required for origin firing
• A mitotic motor protein that separates chromosomes

Correct Answer: An E3 ubiquitin ligase that targets securin and cyclin B for degradation

Q6. The SCF (Skp1–Cullin–F-box) complex primarily contributes to cell-cycle progression by:

• Stabilizing cyclin B during mitosis
• Targeting specific phosphorylated proteins for ubiquitination during G1/S transition
• Directly phosphorylating Rb to release E2F
• Cleaving cohesin to allow sister-chromatid separation

Correct Answer: Targeting specific phosphorylated proteins for ubiquitination during G1/S transition

Q7. Which sensor kinase is predominantly activated by DNA double-strand breaks?

• ATR
• CHK1
• ATM
• mTOR

Correct Answer: ATM

Q8. Activation of checkpoint kinases Chk1 and Chk2 leads to cell-cycle arrest mainly through which mechanism?

• Direct activation of CDK activity
• Phosphorylation and inhibition of Cdc25 phosphatases, preventing CDK activation
• Proteolytic cleavage of cyclins by caspases
• Recruitment of origin recognition complex to DNA

Correct Answer: Phosphorylation and inhibition of Cdc25 phosphatases, preventing CDK activation

Q9. How do Wee1 kinase and Cdc25 phosphatase reciprocally regulate CDK1 activity at the G2/M transition?

• Wee1 removes inhibitory phosphates; Cdc25 adds inhibitory phosphates
• Wee1 adds inhibitory phosphate on CDK1; Cdc25 removes inhibitory phosphate to activate CDK1
• Both Wee1 and Cdc25 ubiquitinate CDK1 to regulate its levels
• Both are transcription factors that repress cyclin B expression

Correct Answer: Wee1 adds inhibitory phosphate on CDK1; Cdc25 removes inhibitory phosphate to activate CDK1

Q10. The spindle assembly checkpoint proteins MAD and BUB delay anaphase onset by:

• Activating separase to cleave cohesin
• Inhibiting APC/C activator Cdc20 until all kinetochores are properly attached
• Dephosphorylating histones to condense chromatin
• Recruiting microtubule severing enzymes

Correct Answer: Inhibiting APC/C activator Cdc20 until all kinetochores are properly attached

Q11. Cyclin D–CDK4/6 complexes promote cell-cycle progression primarily by:

• Phosphorylating Rb to release E2F and permit S-phase gene expression
• Directly initiating DNA replication at origins
• Cleaving cohesin complexes to enable chromosome segregation
• Activating APC/C to degrade S-phase cyclins

Correct Answer: Phosphorylating Rb to release E2F and permit S-phase gene expression

Q12. In flow cytometry DNA content analysis, which DNA content values correspond to G1 and G2/M phases?

• G1 = 4N; G2/M = 2N
• G1 = 1N; G2/M = 2N
• G1 = 2N; G2/M = 4N
• G1 = S-phase; G2/M = sub-G1

Correct Answer: G1 = 2N; G2/M = 4N

Q13. Which statement correctly contrasts the mechanisms of taxanes and vinca alkaloids?

• Taxanes destabilize microtubules whereas vinca alkaloids stabilize them
• Taxanes inhibit DNA polymerase while vinca alkaloids inhibit topoisomerase
• Taxanes stabilize microtubules and inhibit depolymerization; vinca alkaloids prevent microtubule polymerization
• Both drug classes act primarily by inhibiting cyclin-dependent kinases

Correct Answer: Taxanes stabilize microtubules and inhibit depolymerization; vinca alkaloids prevent microtubule polymerization

Q14. What is the principal pharmacological effect of selective CDK4/6 inhibitors in hormone receptor–positive breast cancer?

• Induction of mitotic catastrophe by microtubule stabilization
• Inhibition of Rb phosphorylation resulting in G1 cell-cycle arrest
• Activation of APC/C to promote anaphase onset
• Direct DNA intercalation causing double-strand breaks

Correct Answer: Inhibition of Rb phosphorylation resulting in G1 cell-cycle arrest

Q15. p21 (CIP1/WAF1) regulates the cell cycle by which mechanism?

• Serving as an activating subunit for CDK2
• Acting as a CDK inhibitor that binds cyclin–CDK complexes
• Phosphorylating Rb to promote S phase
• Ubiquitinating cyclins for degradation

Correct Answer: Acting as a CDK inhibitor that binds cyclin–CDK complexes

Q16. Which of the following is a widely used biochemical marker for cellular senescence?

• High Ki-67 proliferation index
• Strong telomerase (hTERT) expression
• Senescence-associated β-galactosidase activity (SA-β-gal)
• Low p16INK4a expression

Correct Answer: Senescence-associated β-galactosidase activity (SA-β-gal)

Q17. Ubiquitin–proteasome–mediated degradation is essential during the cell cycle primarily because it:

• Destroys DNA to allow replication
• Removes specific regulatory proteins like cyclins to permit orderly phase transitions
• Forms the mitotic spindle from ubiquitin-coated tubulin
• Serves as the main energy source in S phase

Correct Answer: Removes specific regulatory proteins like cyclins to permit orderly phase transitions

Q18. Which enzyme directly cleaves cohesin complexes to allow sister-chromatid separation at anaphase?

• Securin
• Separase
• Topoisomerase II
• Proteasome subunit beta

Correct Answer: Separase

Q19. What is “origin licensing” in DNA replication and when does it occur?

• Loading of MCM helicase complexes onto replication origins during G1 to permit later S-phase firing
• Activation of replication origins by CDK phosphorylation during M phase
• Cleavage of origins by nucleases to start replication in G2
• Disassembly of replication forks after completion in G0

Correct Answer: Loading of MCM helicase complexes onto replication origins during G1 to permit later S-phase firing

Q20. Which of the following combination strategies exemplifies rational targeting of the cell cycle in cancer therapy?

• Combining microtubule stabilizers with telomerase activators
• Using CDK4/6 inhibitors together with endocrine therapy (e.g., palbociclib plus letrozole) in ER-positive breast cancer
• Pairing ATM inhibitors with antibiotics to boost immune function
• Administering proteasome inhibitors with growth factor to promote cell proliferation

Correct Answer: Using CDK4/6 inhibitors together with endocrine therapy (e.g., palbociclib plus letrozole) in ER-positive breast cancer

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