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Cell Division

Practice questions on the processes of mitosis and meiosis, including stages, significance, and differences between the two types of cell division.

30 questions

Which factor regulates the exit of cells from mitosis?

Exit from mitosis, defined transition from high CDK1 activity driving chromosome condensation and spindle assembly to low CDK state permitting G1 growth, is regulated primarily by anaphase-promoting complex/cyclosome APC/C ubiquitin ligase. After anaphase onset mediated by APC/C-Cdc20 degradation of securin and cyclin B, second wave of APC/C activity associated with coactivator Cdh1 becomes dominant as CDK1 inactivation allows Cdc14 and PP2A phosphatases to dephosphorylate Cdh1 permitting its binding. APC/C-Cdh1 polyubiquitinates remaining mitotic cyclin B, Polo-like kinase, Aurora kinases A a

Ref: Sullivan & Morgan, Nature Rev Mol Cell Biol 2007, Mitotic Exit Control. Alberts 7th ed., Chapter 17.

What happens during anaphase II of meiosis?

Meiosis consists of two divisions following single S phase, with meiosis II equationally separating sisters after reductional meiosis I segregated homologs. Cells exit meiosis I entering interkinesis without replication, centrosomes duplicate, chromosomes recondense, and spindle reforms often orthogonal to first division axis. At metaphase II plate, sister chromatids align with kinetochores bioriented to opposite poles similar to mitosis, achieved despite haploid chromosome number. Protection of centromeric cohesion established in meiosis I by Shugoshin SGO2 bound to PP2A phosphatase that deph

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 21: Meiosis II Sister Chromatids.

What is the primary function of the centromere during mitosis?

Centromere is specialized chromosomal domain that appears as primary constriction in metaphase chromosomes and functions as essential platform for kinetochore assembly linking chromosomes to spindle microtubules and providing tension sensor. Human centromeres built on megabases of alpha-satellite repeat DNA enriched with nucleosomes containing histone variant CENP-A replacing H3, deposited by chaperone HJURP in G1, epigenetically marking locus independent of sequence alone. CENP-A recruits constitutive centromere-associated network including CENP-C, CENP-I, CENP-H, CENP-T-W-S-X complex forming

Ref: Fukagawa & Earnshaw, Dev Cell 2014, Centromere Function. Alberts 7th ed., Chapter 17, Centromere.

Which of the following proteins is responsible for regulating the G1/S transition?

G1/S transition also known as restriction point in mammals marks commitment to DNA replication independent of extracellular mitogens thereafter. Regulation centers on retinoblastoma protein phosphorylation cascade. Mitogens induce cyclin D-CDK4/6 via Ras-MAPK pathway which initiates partial phosphorylation of Rb family proteins pRb, p107, p130 at specific serine sites, displacing histone deacetylases and allowing transcription of cyclin E gene driven by E2F1-3. Cyclin E then associates with CDK2, activated by CAK phosphorylation, forming cyclin E-CDK2 holoenzyme that hyperphosphorylates Rb at

Ref: Dulic et al., Cell 1992, Cyclin E-CDK2 at G1/S. Alberts 7th ed., Chapter 17, Restriction Point Control.

Which phase of the cell cycle is referred to as the quiescent phase?

Quiescent phase G0 represents reversible exit from cell cycle distinct from terminal differentiation and senescence, providing flexible pause aligning proliferation with physiological needs. Cells enter G0 from early G1 when mitogens withdraw, contact inhibition activates Hippo signaling with YAP nuclear exclusion, or nutrient deprivation suppresses mTORC1. Molecularly, cyclin D transcription declines, p27Kip1 and p130 Rb2 pocket protein accumulate, assembling DREAM complex with E2F4-DP1 repressing over 800 cell cycle genes including cyclin A, cyclin B, MCM helicases, and PCNA. Ribosomal RNA t

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 17: G0 and Quiescence Regulation.

What ensures that DNA damage is repaired before mitosis?

Faithful genome transmission requires that DNA lesions incurred during replication or from external mutagens be repaired before chromosomes condense and segregate to avoid transmitting broken chromosomes and rearrangements. G2/M checkpoint serves this function by integrating damage sensing with CDK1 control. Lesions such as double-strand breaks recruit MRN complex MRE11-RAD50-NBS1 that activates ATM kinase, while RPA-coated single-stranded DNA from resection or stalled forks recruits ATRIP-ATR and TopBP1 activator. Effector kinases Chk2 and Chk1 phosphorylate dual-specificity phosphatases Cdc2

Ref: Sancar et al., Annu Rev Biochem 2004, DNA Repair Checkpoints. Alberts 7th ed., Chapter 17, G2/M Damage Control.

Individual chromosomes are clearly visible in which phase?

Visibility of individual chromosomes under light microscope depends on degree of condensation regulated by condensin complexes and histone modifications across cell cycle. Interphase chromatin exists as 10 nanometer beads-on-string fiber further folded into 30 nanometer fiber and looped domains anchored to nuclear matrix, occupying distinct chromosome territories where active transcription and replication occur, but overlapping extensively making individual chromosomes unresolvable. Entry into M phase, triggered by cyclin B-CDK1 rising activity, activates condensin I and II ATPases that extrud

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 17: Mitotic Chromosome Condensation.

How many kinetochores are present in a human cell at mitosis?

Kinetochore count reflects chromosome and chromatid numbers fundamental to ploidy understanding. Human diploid somatic cell harbors 46 chromosomes, each defined by single centromere region where kinetochore assembles providing attachment site to spindle microtubules and checkpoint signaling platform. In G1, each chromosome contains one chromatid and one functional centromere kinetochore assembly site. During S phase, DNA replication converts each chromosome into two sister chromatids held together by cohesin, each sister chromatid retains its own centromere capable of assembling independent ki

Ref: Cleveland et al., Cell 2003, Centromere and Kinetochore Number. Alberts 7th ed., Chapter 17.

The site of the division plane during cytokinesis in animal cells is determined by:

Cytokinesis in animal cells determines placement of furrow such that daughter cells inherit single genome copy and appropriate cytoplasmic volume. Experimental embryology demonstrated furrow forms where central spindle contacts cortex. Mechanistically, anaphase central spindle assembled from overlapping antiparallel interpolar microtubules bundled by PRC1 and centralspindlin component KIF4 recruits centralspindlin heterotetramer consisting of kinesin MKLP1 and RhoGAP MgcRacGAP. Centralspindlin clusters ECT2 RhoGEF, generating zone of active RhoA-GTP precisely at equatorial membrane. RhoA-GTP a

Ref: Fededa & Gerlich, Current Biology 2012, Division Plane Specification. Alberts 7th ed., Chapter 17.

What happens if a proteasome inhibitor is added to cells in G2 phase?

Cell cycle progression relies heavily on ubiquitin-proteasome pathway to confer irreversibility to transitions via degradation of cyclins and CDK inhibitors. Proteasome comprises 20S catalytic core with chymotrypsin-like, trypsin-like, caspase-like activities and 19S regulatory particle recognizing polyubiquitinated proteins. Inhibitors such as MG132 peptide aldehyde, lactacystin, and clinically used bortezomib block catalytic threonine residues, causing accumulation of polyubiquitinated substrates. When applied in G2, proteasome blockade prevents degradation of SCF substrates like p21 and Wee

Ref: Ciechanover, Nature Reviews Mol Cell Biol 2005, Proteasome and Cycle. Alberts 7th ed., Chapter 3.

Which phase of mitosis is characterized by nuclear envelope reformation?

Telophase reverses many mitotic changes to re-establish interphase nuclear architecture in daughter cells following sister chromatid arrival at poles. Decline in cyclin B levels due to APC/C-Cdh1 mediated proteolysis extinguishes CDK1 activity, allowing protein phosphatases PP1 recruited to kinetochores by Repo-Man and PP2A-B55 to dephosphorylate key substrates. Dephosphorylation causes dissociation of condensin I and II complexes leading to chromatin decondensation and transcriptional restart, reassembly of nuclear lamina from lamin A/C and B1/B2 depolymerized during prophase, recruitment of

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 17: Telophase Restoration.

What is the function of the spindle assembly checkpoint?

Reliability of chromosome segregation depends on surveillance mechanism preventing anaphase until every chromosome correctly attached to spindle, because single missegregation yields aneuploid daughter prone to tumor development or cell death. Spindle assembly checkpoint monitors occupancy and tension at kinetochores, large protein structures assembled on CENP-A containing centromeric chromatin. Unattached kinetochores recruit Mad1-Mad2 complex that catalyzes conversion of cytosolic open Mad2 to closed form bound to Cdc20. Together with BubR1, Bub3, Mps1-phosphorylated Bub1 they assemble mitot

Ref: Musacchio & Salmon, Nature Reviews Mol Cell Biol 2007, SAC Mechanism. Alberts 7th ed., Chapter 17.