Part 5 — Cell Cycle Control, Cyclins/CDKs, Checkpoints & Cancer (Q101–125)

Part 5 — Cell Cycle Control, Cyclins/CDKs, Checkpoints & Cancer (Q101–125)

Q101.

Which molecule directly activates cyclin-dependent kinases (CDKs)?
A. DNA polymerase
B. Cyclins ✅
C. Histones
D. Topoisomerase

Explanation:

• A. DNA polymerase: Enzyme of DNA replication, not CDK regulator.
• B. Cyclins (Correct): Bind CDKs to form active kinase complexes.
• **C. Histones: DNA packaging proteins, not CDK activators.
• **D. Topoisomerase: relieves supercoiling in DNA.

Q102.

The key regulator of G1 to S phase transition is:
A. Cyclin D/CDK4
B. Cyclin E/CDK2 ✅
C. Cyclin A/CDK1
D. Cyclin B/CDK1

Explanation:

• **A. Cyclin D/CDK4: drives G1 progression.
• **B. Cyclin E/CDK2 (Correct): essential for crossing the restriction point (R-point).
• **C. Cyclin A/CDK1: involved in S/G2.
• **D. Cyclin B/CDK1: triggers mitosis.

Q103.

The protein that prevents S-phase entry by binding and inhibiting E2F is:
A. p53
B. Retinoblastoma protein (Rb) ✅
C. Cyclin B
D. APC/C

Explanation:

• **A. p53: DNA damage checkpoint, not E2F.
• **B. Rb (Correct): binds E2F transcription factor, blocking S-phase genes until phosphorylated.
• **C. Cyclin B: mitotic regulator.
• **D. APC/C: regulates anaphase, not S-phase.

Q104.

Which checkpoint ensures damaged DNA does not replicate?
A. G1/S checkpoint ✅
B. G2/M checkpoint
C. Metaphase checkpoint
D. Cytokinesis checkpoint

Explanation:

• A. G1/S (Correct): Prevents replication if DNA is damaged.
• **B. G2/M: checks for replication completion.
• **C. Metaphase: ensures spindle attachment.
• **D. Cytokinesis checkpoint: not standard.

Q105.

The tumor suppressor gene often mutated in cancers is:
A. p21
B. p53 ✅
C. Rb
D. BRCA2

Explanation:

• **A. p21: CDK inhibitor, regulated by p53.
• B. p53 (Correct): “Guardian of the genome,” mutated in >50% of cancers.
• **C. Rb: also a tumor suppressor, but less common.
• **D. BRCA2: repair gene, linked to breast cancer.

Q106.

p21 protein inhibits:
A. Cyclin degradation
B. CDK activity ✅
C. DNA replication enzymes
D. Telomerase

Explanation:

• **A. Not cyclin degradation.
• **B. Correct — p21 is a CDK inhibitor induced by p53.
• **C. Does not directly inhibit DNA polymerases.
• **D. Not related to telomerase.

Q107.

The G2/M checkpoint is important to:
A. Prevent replication errors from being passed into mitosis ✅
B. Ensure spindle attachment
C. Check nutrient availability
D. Stop apoptosis

Explanation:

• **A. Correct — verifies DNA fully replicated & intact.
• **B. Spindle checkpoint = metaphase.
• **C. Nutrients: checked at G1/S.
• **D. Apoptosis not a checkpoint.

Q108.

The spindle assembly checkpoint halts the cell cycle until:
A. DNA replication is completed
B. Chromosomes attach properly to spindle fibers ✅
C. Cytokinesis begins
D. Telomeres are repaired

Explanation:

• **A. DNA replication = G2/M.
• **B. Correct — prevents anaphase until all kinetochores attached.
• **C. Cytokinesis = after mitosis.
• **D. Telomeres not checked here.

Q109.

Overexpression of cyclin D may result in:
A. Cell cycle arrest
B. Tumorigenesis ✅
C. Apoptosis
D. DNA repair

Explanation:

• **A. Not arrest, opposite effect.
• **B. Correct — leads to uncontrolled progression through G1 → cancer.
• **C. Apoptosis suppressed, not induced.
• **D. Repair unrelated.

Q110.

The enzyme complex responsible for sister chromatid separation is activated by:
A. p53
B. Anaphase-promoting complex (APC/C) ✅
C. Cyclin D/CDK4
D. Topoisomerase

Explanation:

• **A. p53: DNA damage checkpoint.
• **B. APC/C (Correct): degrades securin → activates separase → cohesin cleavage.
• **C. Cyclin D: early G1.
• **D. Topoisomerase: DNA coiling.

Q111.

Which protein phosphorylates Rb, releasing E2F?
A. Cyclin D/CDK4 ✅
B. APC/C
C. p53
D. p21

Explanation:

• **A. Correct — phosphorylated Rb releases E2F → S-phase entry.
• **B. APC/C: anaphase control.
• **C. p53: DNA damage, apoptosis.
• **D. p21: inhibits CDKs.

Q112.

Cyclin B/CDK1 complex is also called:
A. MPF (Maturation Promoting Factor) ✅
B. APC/C
C. Rb protein
D. Separase

Explanation:

• **A. Correct — triggers mitosis entry.
• **B. APC/C: anaphase trigger.
• **C. Rb: tumor suppressor.
• **D. Separase: cleaves cohesins.

Q113.

Which is the role of ubiquitin-proteasome pathway in cell cycle control?
A. DNA replication
B. Cyclin degradation ✅
C. Cohesin cleavage
D. RNA transcription

Explanation:

• **A. Not replication.
• **B. Correct — ubiquitination tags cyclins for proteasome degradation, ensuring transitions.
• **C. Cohesin cleavage is separase-mediated.
• **D. RNA transcription regulated by other factors.

Q114.

Inactivation of Rb protein causes:
A. Arrest at G1/S
B. Uncontrolled entry into S phase ✅
C. Apoptosis
D. Halt at G2/M

Explanation:

• **A. Active Rb = arrest, inactive = release.
• **B. Correct — loss of Rb function → unregulated S-phase entry.
• **C. Not directly apoptosis.
• **D. Not G2/M role.

Q115.

Which is true for p53 in response to DNA damage?
A. Activates Rb phosphorylation
B. Induces p21 expression ✅
C. Degrades cyclins
D. Cleaves cohesins

Explanation:

• **A. Opposite effect.
• **B. Correct — p53 → p21 → CDK inhibition → cell cycle arrest.
• **C. Cyclin degradation mainly by APC/C.
• **D. Cohesin cleavage by separase.

Q116.

Mutation in which checkpoint protein is most directly linked to colon cancer (Li-Fraumeni syndrome)?
A. p53 ✅
B. Rb
C. APC/C
D. p21

Explanation:

• **A. Correct — Li-Fraumeni syndrome arises from p53 mutation.
• **B. Rb mutation: retinoblastoma.
• **C. APC/C mutation: colon polyps, but Li-Fraumeni is p53.
• **D. p21: downstream of p53.

Q117.

Which drug stabilizes microtubules, preventing anaphase, and is used in cancer chemotherapy?
A. Colchicine
B. Paclitaxel (Taxol) ✅
C. Vinblastine
D. Methotrexate

Explanation:

• **A. Colchicine: prevents polymerization.
• **B. Taxol (Correct): stabilizes microtubules → no depolymerization.
• **C. Vinblastine: depolymerizes MTs.
• **D. Methotrexate: folate antagonist.

Q118.

Apoptosis is triggered if DNA damage is irreparable, mainly by:
A. Cyclin B
B. Caspases ✅
C. APC/C
D. Separase

Explanation:

• **A. Cyclin B: mitosis trigger, not apoptosis.
• **B. Caspases (Correct): proteases executing programmed cell death.
• **C. APC/C: mitosis regulator.
• **D. Separase: chromatid separation.

Q119.

Which checkpoint is most critical for preventing cancer development?
A. G1/S ✅
B. G2/M
C. Spindle checkpoint
D. Cytokinesis checkpoint

Explanation:

• **A. Correct — ensures damaged DNA does not replicate.
• **B. G2/M important but less primary.
• **C. Prevents aneuploidy, not mutation propagation.
• **D. Not a major checkpoint.

Q120.

In chronic myeloid leukemia, a translocation creates the “Philadelphia chromosome,” which fuses:
A. BCR and ABL genes ✅
B. Rb and p53
C. BRCA1 and BRCA2
D. Cyclin and CDK

Explanation:

• **A. Correct — BCR-ABL fusion → constitutive tyrosine kinase activity.
• **B. Not involved.
• **C. BRCA = breast cancer repair genes.
• **D. Not gene fusion.

Q121.

The restriction point (R-point) is located in:
A. G1 phase ✅
B. S phase
C. G2 phase
D. M phase

Explanation:

• **A. Correct — R-point in late G1 decides whether cell enters S or exits into G0.
• B/C/D. Not the R-point location.

Q122.

Cyclin A is mainly associated with:
A. G1 progression
B. S-phase progression ✅
C. Mitosis entry
D. Cytokinesis

Explanation:

• **A. G1: Cyclin D.
• **B. Correct — Cyclin A/CDK2 promotes DNA replication in S-phase.
• **C. Cyclin B/CDK1 triggers mitosis.
• **D. Cytokinesis is actin-driven.

Q123.

Which process is a direct consequence of APC/C activation?
A. Telomere extension
B. Degradation of securin ✅
C. p21 induction
D. CDK inhibition

Explanation:

• **A. Telomerase: unrelated.
• **B. Correct — securin degraded → separase activated → chromatid separation.
• **C. p21 induction: p53.
• **D. CDK inhibition: CKIs.

Q124.

Which mutation leads to hereditary retinoblastoma?
A. Rb gene ✅
B. p53 gene
C. BRCA1 gene
D. Cyclin E gene

Explanation:

• **A. Correct — Rb mutation → uncontrolled S-phase entry → eye tumors.
• **B. p53 = Li-Fraumeni syndrome.
• **C. BRCA1 = breast/ovarian cancer predisposition.
• **D. Cyclin E: regulator, not common inherited cancer gene.

Q125.

The protein ATM (Ataxia Telangiectasia Mutated) is activated by:
A. Microtubule assembly
B. DNA double-strand breaks ✅
C. Cyclin degradation
D. Apoptosis

Explanation:

• **A. Not MT-related.
• **B. Correct — ATM kinase senses double-strand DNA breaks, activates p53 pathway.
• **C. Cyclin degradation: proteasome.
• **D. ATM acts upstream of apoptosis.

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