60 free MCQs on Cell Cycle and Cell Division with worked answers and explanations. Mitosis and meiosis: how cells divide for growth, repair, and reproduction.
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The cell cycle: G1 (growth and preparation), S (DNA replication, chromosome number stays 2n but DNA content doubles), G2 (final checks before division), and M (mitosis itself) — together, G1+S+G2 make up interphase.
Q1.
Mitosis produces how many daughter cells?
Answer: B. 2
Why: Mitosis produces 2 genetically identical daughter cells, each with the same chromosome number as the parent cell.
Q2.
Meiosis produces how many daughter cells?
Answer: C. 4
Why: Meiosis produces 4 haploid daughter cells (each with half the chromosome number of the parent).
Q3.
The purpose of meiosis is:
Answer: B. Production of gametes (sex cells)
Why: Meiosis produces gametes (sperm and eggs) with half the chromosome number, enabling sexual reproduction.
Q4.
DNA replication occurs during which phase of the cell cycle?
Answer: B. S phase (Synthesis)
Why: DNA replication occurs during S phase (Synthesis phase) of interphase, before cell division begins.
Q5.
In mitosis, chromosomes line up at the cell's equator during:
Answer: B. Metaphase
Why: Metaphase: chromosomes align at the metaphase plate (cell's equator) attached to spindle fibers.
Q6.
During anaphase of mitosis:
Answer: C. Sister chromatids separate and move to poles
Why: Anaphase: sister chromatids separate as spindle fibers pull them to opposite poles.
Q7.
The correct sequence of mitotic phases is:
Answer: A. PMAT
Why: PMAT: Prophase, Metaphase, Anaphase, Telophase. A helpful mnemonic for the stages of mitosis.
Q8.
Crossing over occurs during which phase of meiosis?
Answer: C. Prophase I
Why: Crossing over (exchange of DNA between homologous chromosomes) occurs during Prophase I of meiosis. It generates genetic variation.
Q9.
Homologous chromosomes separate during:
Answer: B. Meiosis I anaphase
Why: Homologous chromosomes separate during Anaphase I (Meiosis I). Sister chromatids separate during Anaphase II.
Q10.
Cancer is characterized by:
Answer: C. Uncontrolled cell division (mitosis)
Why: Cancer results from loss of cell cycle control: cells divide uncontrollably, forming tumors.
Q11.
A human body cell has 46 chromosomes. After meiosis, gametes have:
Answer: C. 23
Why: Meiosis halves chromosome number. Human gametes (sperm/egg) have 23 chromosomes (haploid).
Q12.
Telophase is characterized by:
Answer: C. Reformation of nuclear envelope
Why: Telophase: nuclear envelope reforms around chromosomes at each pole; chromosomes begin to decondense.
Q13.
Cytokinesis in animal cells involves:
Answer: B. Cleavage furrow
Why: In animal cells, a cleavage furrow forms and pinches the cell in two. Plant cells form a cell plate from the inside out.
Q14.
Prophase of mitosis is characterized by:
Answer: C. Chromosomes condense and become visible
Why: Prophase: chromatin condenses into visible chromosomes; nuclear envelope begins to break down; spindle forms.
Q15.
What is the ploidy of a cell after meiosis I?
Answer: C. Haploid (n)
Why: After Meiosis I, cells are haploid (n) but with sister chromatids still joined. Meiosis II separates the chromatids.
Q16.
The spindle apparatus is made of:
Answer: B. Microtubules
Why: Spindle fibers are made of microtubules (tubulin protein). They attach to chromosomes at kinetochores and pull them to poles.
Q17.
Interphase is:
Answer: B. The phase between divisions (G1, S, G2)
Why: Interphase (G1 + S + G2) is the longest phase. Cell grows, copies DNA, and prepares for division.
Q18.
Bivalent is formed during meiosis I when:
Answer: B. Homologous chromosomes pair up (synapsis)
Why: Bivalent (tetrad): two homologous chromosomes pair up (synapsis) in Prophase I. Each homolog consists of two sister chromatids.
Q19.
Checkpoint controls in the cell cycle ensure:
Answer: B. DNA is correctly replicated and chromosomes properly aligned before proceeding
Why: Cell cycle checkpoints (G1, S, G2/M, spindle) monitor DNA integrity and proper chromosome attachment. Damaged cells don't proceed.
Q20.
Programmed cell death is called:
Answer: C. Apoptosis
Why: Apoptosis is programmed cell death: an orderly process by which cells self-destruct when they are damaged or no longer needed.
Q21.
The G2 checkpoint ensures:
Answer: A. DNA is replicated without errors before mitosis
Why: G2 checkpoint: verifies DNA replication is complete and error-free before entering mitosis. Damaged DNA triggers arrest.
Q22.
Kinetochores are protein complexes that:
Answer: B. Attach spindle microtubules to chromosomes at centromeres
Why: Kinetochores are protein complexes on the centromere of each chromatid. Spindle microtubules attach here to pull chromosomes apart.
Q23.
MPF (Maturation Promoting Factor) promotes:
Answer: B. Entry into mitosis (G2 to M transition)
Why: MPF (Cyclin B + Cdk1 complex) promotes entry into mitosis. It was the first cell cycle control protein discovered.
Q24.
Endoreduplication results in:
Answer: B. Polyploid cells (multiple sets of chromosomes)
Why: Endoreduplication: DNA replicates without cell division, producing polyploid cells. Common in plant cells and some animal tissues.
Q25.
Karyokinesis refers to:
Answer: B. Nuclear division
Why: Karyokinesis = nuclear division (division of the nucleus). Cytokinesis = division of the cytoplasm.
Q26.
Nondisjunction during meiosis I results in:
Answer: B. Gametes with both homologs or neither (n+1 and n-1)
Why: Nondisjunction at Meiosis I: both homologs go to same cell. Results in n+1 and n-1 gametes. Leads to monosomy or trisomy.
Q27.
Down syndrome (Trisomy 21) is caused by:
Answer: B. Extra copy of chromosome 21 (nondisjunction)
Why: Down syndrome: extra copy of chromosome 21 (2n+1 = 47). Most often caused by nondisjunction during maternal meiosis I.
Q28.
Cyclin proteins control the cell cycle by:
Answer: B. Activating Cdks (cyclin-dependent kinases) at specific stages
Why: Cyclins rise and fall during the cell cycle. They activate Cdks, which phosphorylate target proteins to drive cell cycle progression.
Q29.
Chiasmata are visible sites of:
Answer: B. Crossing over (genetic recombination) in Prophase I
Why: Chiasmata are the X-shaped crossing points where homologous chromosomes have exchanged DNA. They hold bivalents together.
Q30.
Which cancer suppressor gene is mutated in many cancers?
Answer: B. p53 (the guardian of the genome)
Why: p53 is a tumor suppressor protein. Mutated in >50% of human cancers. It normally stops cell cycle or triggers apoptosis when DNA is damaged.
Q31.
During meiosis II, sister chromatids separate similar to:
Answer: B. Mitosis anaphase (anaphase II)
Why: Meiosis II separates sister chromatids exactly like mitosis (anaphase II = mitotic anaphase), producing haploid cells.
Q32.
Spindle assembly checkpoint monitors:
Answer: B. Correct attachment of all chromosomes to spindle fibers
Why: Spindle assembly checkpoint: holds the cell at metaphase until ALL chromosomes are properly attached to spindle at kinetochores.
Q33.
Telomere shortening is associated with:
Answer: B. Normal cellular aging and senescence
Why: Telomeres shorten with each cell division. When critically short, cells enter senescence or apoptosis. This contributes to aging.
Q34.
Amitosis is:
Answer: B. Direct cell division (simple fission, no spindle)
Why: Amitosis: direct cell division by simple constriction of the nucleus without spindle formation. Seen in some lower organisms.
Q35.
The mitotic index is used to measure:
Answer: B. Proportion of cells in mitosis (used in cancer diagnosis)
Why: Mitotic index = (cells in mitosis) / (total cells). High mitotic index indicates rapid cell division. Used in cancer staging.
Q36.
Recombination frequency between two genes indicates:
Answer: B. Distance between genes on the same chromosome
Why: Recombination frequency (crossover frequency) is proportional to the distance between linked genes. Used to construct genetic maps (1 cM = 1% recombination).
Q37.
Cells that have left the cell cycle to perform specialized functions are in:
Answer: C. G0 phase (quiescent state)
Why: G0 phase: cells exit the cell cycle and enter a quiescent state. Many differentiated cells (neurons, muscle) are in G0.
Q38.
During zygotene of meiosis I, homologous chromosomes:
Answer: C. Begin to pair (synapsis starts)
Why: Zygotene: homologous chromosomes begin to pair (synapsis) along their entire length, forming bivalents.
Q39.
Turner syndrome (45,X) results from:
Answer: B. Missing X chromosome (monosomy X: nondisjunction)
Why: Turner syndrome: females with 45,X (one X chromosome instead of two). Caused by nondisjunction. Short stature, infertile, no secondary sexual development.
Q40.
Actin and myosin are involved in which step of cell division?
Answer: C. Cytokinesis (cleavage furrow formation)
Why: Actin and myosin form the contractile ring in animal cell cytokinesis. The ring contracts to form the cleavage furrow.
Q41.
Aurora kinase B is involved in:
Answer: B. Chromosome segregation error correction at kinetochores
Why: Aurora B kinase is part of the chromosomal passenger complex (CPC). It corrects erroneous kinetochore-microtubule attachments (e.g., merotelic) to prevent mis-segregation.
Q42.
The SAC (spindle assembly checkpoint) is satisfied when:
Answer: B. Every kinetochore has tension from being attached to microtubules from opposite poles
Why: SAC is silenced only when ALL kinetochores have amphitelic (bioriented) attachments generating tension. Mad2 is released from kinetochores, allowing APC/C activation.
Q43.
Securin prevents premature sister chromatid separation by:
Answer: B. Inhibiting separase (which would cleave cohesin)
Why: Securin inhibits separase. At anaphase onset, APC/C degrades securin, freeing separase to cleave cohesin Scc1 subunit, triggering sister chromatid separation.
Q44.
The retinoblastoma protein (Rb) controls the cell cycle by:
Answer: B. Binding E2F transcription factors, blocking S phase entry until phosphorylated by Cyclin D/Cdk4
Why: Rb protein sequesters E2F transcription factors. Cyclin D/Cdk4 (and Cdk6) phosphorylate Rb, releasing E2F to activate S-phase genes. This is the critical G1 to S transition.
Q45.
Aneuploidy most commonly results from:
Answer: B. Spindle assembly checkpoint failure causing chromosome mis-segregation
Why: Aneuploidy (abnormal chromosome number) most commonly arises from SAC failure or cohesion defects causing unequal chromosome segregation during mitosis or meiosis.
Q46.
The transition from metaphase to anaphase in mitosis requires:
Answer: B. APC/C (anaphase-promoting complex) activation by Cdc20, degrading cyclin B and securin
Why: APC/C-Cdc20 ubiquitinates cyclin B (inactivating CDK1) and securin (releasing separase). Both are degraded by the proteasome, triggering anaphase.
Q47.
Merotelic attachment is dangerous in cell division because:
Answer: B. One kinetochore is attached to microtubules from BOTH poles, risking lagging chromosomes in anaphase
Why: Merotelic attachment: one kinetochore attached to both spindle poles. Not detected by SAC. Can lead to lagging chromosomes and aneuploidy. Corrected by Aurora B kinase.
Q48.
Telomerase activity is high in:
Answer: B. Cancer cells and embryonic stem cells
Why: Telomerase adds telomeric repeats to prevent shortening. Active in germ cells, stem cells, and most cancer cells (enabling their immortality).
Q49.
Condensin I and II differ in:
Answer: B. Condensin I works in cytoplasm during mitosis; condensin II works in nucleus from G2 onward for different aspects of chromosome architecture
Why: Condensin II is nuclear, loads in prophase for axial compaction. Condensin I is cytoplasmic until nuclear envelope breaks down, loading for lateral compaction. Together they shape mitotic chromosomes.
Q50.
The pachytene checkpoint in meiosis monitors:
Answer: B. Synapsis completion and DNA double-strand break repair
Why: Pachytene checkpoint: monitors completion of synapsis and repair of meiotic DSBs (programmed by Spo11) before cells can proceed to metaphase I.
Q51.
Proteolysis of geminin at the end of mitosis allows:
Answer: B. Pre-replication complex (pre-RC) assembly licensing new DNA replication in G1
Why: Geminin inhibits Cdt1, blocking pre-RC assembly. APC/C degrades geminin in late mitosis, allowing Cdt1 to re-license origins for the next S phase.
Q52.
Which kinase phosphorylates histone H3 at Serine 10 during mitosis?
Answer: B. Aurora B kinase
Why: Aurora B kinase phosphorylates histone H3 at Ser10 during mitosis. This is a widely used marker for cells in mitosis in immunofluorescence.
Q53.
Cohesion between sister chromatids is established during:
Answer: B. S phase (DNA replication)
Why: Cohesin rings are loaded onto chromosomes and establish sister chromatid cohesion during DNA replication in S phase.
Q54.
In meiosis, the protein SYCP3 is a component of:
Answer: B. The synaptonemal complex (SC) that forms between homologs in Prophase I
Why: SYCP3 is a structural component of the lateral elements of the synaptonemal complex, the proteinaceous structure that holds homologs together during meiosis I.
Q55.
Gene conversion during meiotic recombination results in:
Answer: B. Non-reciprocal transfer: one allele replaced by sequence from homolog
Why: Gene conversion: during DSB repair in meiosis, the broken strand uses the homolog as a template. One allele can be converted to the other sequence non-reciprocally.
Q56.
The Holliday junction in recombination is:
Answer: B. A four-way DNA junction formed during crossing-over (resolved to form crossover or non-crossover products)
Why: Holliday junction: four-stranded structure formed by branch migration during recombination. Resolution by resolvases determines if crossover (CO) or non-crossover (NCO) outcome.
Q57.
Polo-like kinase 1 (PLK1) functions in:
Answer: B. Multiple mitotic steps: centrosome maturation, APC/C activation, kinetochore function, cytokinesis
Why: PLK1 has multiple roles: centrosome separation, spindle assembly, chromosome segregation via kinetochore function, and cytokinesis initiation.
Q58.
Chromosomal instability (CIN) in cancer cells is linked to:
Answer: B. Centrosome amplification and defective SAC leading to ongoing mis-segregation
Why: CIN: ongoing chromosomal mis-segregation in cancer cells. Often caused by centrosome amplification (multipolar spindles), defective SAC, or kinetochore attachment errors.
Q59.
The abscission step of cytokinesis in animal cells involves:
Answer: B. Plasma membrane fusion and cutting at the midbody region (ESCRT machinery)
Why: Abscission: the final cut of cytoplasm connecting two daughter cells. ESCRT-III machinery at the midbody constricts and cuts the narrow cytoplasmic bridge.
Q60.
Mitotic slippage occurs when:
Answer: B. Cells exit mitosis without completing cell division (due to slow APC/C activation) and become aneuploid
Why: Mitotic slippage: slow degradation of cyclin B (despite SAC) eventually drops CDK1 activity below the threshold. Cell exits mitosis prematurely without division, generating aneuploid daughter or tetraploid cell.