D2.1 Cell and nuclear division

Cell and nuclear division coordinate DNA replication, chromosome movement, cytokinesis, meiosis, cell-cycle control and proliferation to produce new cells in organisms.

Learning objectives

D2.1.1Generation of new cells• All cells arise from pre-existing parent cells by cell division• Division produces daughter cells for growth, replacement, repair, or reproduction D2.1.2Cytokinesis• Cytokinesis splits cytoplasm after nuclear division• Animal cells use a contractile ring; plant cells form a vesicle-derived cell plate D2.1.3Equal and unequal cytokinesis• Equal cytokinesis gives daughter cells similar amounts of cytoplasm• Unequal cytokinesis occurs in oogenesis and yeast budding D2.1.4Roles of mitosis and meiosis• Mitosis maintains chromosome number for growth, repair, and asexual reproduction• Meiosis halves chromosome number for gametes and generates genetic diversity D2.1.5DNA replication prerequisite• DNA replication in interphase produces chromosomes with sister chromatids• Sister chromatids remain joined at centromeres until separation D2.1.6Shared features• Mitosis and meiosis both condense chromatin into movable chromosomes• Histones, nucleosomes, spindle microtubules, and motor proteins organize movement D2.1.7Phases of mitosis• Prophase condenses chromosomes; metaphase aligns them at the equator• Anaphase separates chromatids; telophase reforms nuclei, producing identical nuclei D2.1.8Identification of mitosis phases• Mitosis phases are identified in diagrams, micrographs, and root-tip squashes• Chromosome condensation, equator alignment, separation, and nuclear membranes are cues D2.1.9Meiosis as reduction division• Meiosis has two nuclear divisions after one round of DNA replication• Homologous chromosomes separate in meiosis I, producing haploid nuclei D2.1.10Down syndrome• Non-disjunction is failed separation of homologues or sister chromatids in meiosis• Down syndrome usually results from trisomy 21 after non-disjunction D2.1.11Meiosis generates variation• Crossing over at chiasmata exchanges DNA between non-sister chromatids• Random orientation of bivalents and fertilization create new allele combinations D2.1.12(HL)—Cell proliferation• Cell proliferation increases cell number by repeated mitosis• Examples include plant meristems, early embryos, skin replacement, and wound healing D2.1.13(HL)—Cell cycle phases• The cell cycle includes interphase, mitosis, and cytokinesis• Interphase has G1 growth, S-phase DNA replication, and G2 preparation D2.1.14(HL)—Cell growth during interphase• Interphase is metabolically active, not a resting state• Cells synthesize proteins, replicate DNA, grow cytoplasm, and increase organelles D2.1.15(HL)—Cell cycle control by cyclins• Cyclin concentrations rise and fall to activate cyclin-dependent kinases• CDK-cyclin complexes such as MPF control checkpoints and mitosis entry D2.1.16(HL)—Mutations in cell cycle genes• Proto-oncogene activation and tumour suppressor loss disrupt checkpoints• Accumulated mutations can cause uncontrolled proliferation and cancer D2.1.17(HL)—Tumour differences• Benign tumours grow locally; malignant tumours invade neighbouring tissues• Metastasis spreads cancer cells to form secondary tumours

Every new cell arises when a pre-existing parent cell divides. The daughter cells inherit cellular material and DNA from that lineage; they are not assembled from non-living parts.

Cell division supplies new cells for:

growth of a multicellular organism
replacement of worn or damaged cells
tissue repair after injury
reproduction in unicellular organisms and some multicellular organisms

Cell division increases cell number. Growth of an individual cell increases cell size; organisms often require both processes.

One parent cell divides by mitosis into daughter cells that contribute to growth, tissue repair, cell replacement or asexual reproduction.

Cytokinesis partitions the cytoplasm after nuclear division so the daughter nuclei become separate cells.

Feature	Animal cell	Plant cell
starting constraint	flexible plasma membrane	rigid existing cell wall
mechanism	actin–myosin contractile ring tightens a cleavage furrow	Golgi-derived vesicles fuse at the equator
result	membrane pinches inward	cell plate becomes new membranes and wall between daughters

Both mechanisms divide one cytoplasm around two daughter nuclei, but they solve the mechanical problem in opposite directions: inward constriction versus construction from the centre outward.

Animal-cell cytokinesis uses a cleavage furrow, whereas plant-cell cytokinesis joins vesicles into a central cell plate.

Cytokinesis often gives daughter cells similar cytoplasmic volumes, but the partition can be unequal when the daughters have different immediate functions.

Oogenesis: one cell retains most cytoplasm, organelles and stored nutrients to become the ovum; small polar bodies mainly remove extra chromosome sets.
Yeast budding: a smaller bud grows from the parent and separates after receiving a nucleus and essential cell components.

Unequal cytokinesis refers to cytoplasmic allocation, not deliberately unequal chromosome inheritance. Normal daughter nuclei still require the appropriate chromosome set.

Equal cytokinesis is contrasted with a large oocyte and polar body and with a small yeast bud on a larger parent cell.

Dimension	Mitosis	Meiosis
nuclear divisions	one	two after one DNA replication
usual nuclei produced	two	four
chromosome number	maintained	halved
genetic relationship	normally identical to parent and each other	varied combinations
main roles	growth, replacement, repair, asexual reproduction	production of cells that develop into gametes

Diploid (2n) nuclei contain two homologous sets of chromosomes. Haploid (n) nuclei contain one set.

Mitosis and meiosis are nuclear divisions. Cytokinesis is the separate division of cytoplasm that usually follows.

A diploid parent produces two genetically similar diploid nuclei by mitosis or four genetically varied haploid nuclei by meiosis.

Before S phase, one chromosome contains one DNA molecule. During S phase that DNA is replicated.

An unreplicated chromosome becomes two sister chromatids joined at a centromere and later separates into daughter chromosomes.

After replication, the chromosome consists of two nearly identical sister chromatids joined at a centromere. The chromosome count has not doubled, but the DNA amount has.

When the sister chromatids separate, each becomes an individual daughter chromosome. Sending one copy to each future nucleus preserves a complete genome.

Do not count chromatids as separate chromosomes while they remain joined at one centromere.

Each chromosome is one very long DNA molecule. Accurate division requires it to be packaged into a compact unit and attached to machinery that can position and separate it.

Mitosis and meiosis share three mechanical features:

DNA wrapped around histones and nucleosomes condenses into chromosomes.
Spindle microtubules attach through centromere-associated structures.
Microtubule dynamics and motor proteins position and move chromosomes.

Condensation does not copy DNA. It changes packaging so long molecules can move with less tangling or breakage.

DNA wraps around histones into chromatin, condenses into a duplicated chromosome and attaches at the centromere region to spindle microtubules.

Prophase: chromatin condenses into visible duplicated chromosomes; the nucleolus disappears, the nuclear envelope breaks down, and the spindle forms.

Metaphase: spindle microtubules attach to the centromere region from opposite poles and position chromosome centromeres at the cell equator.

Identification cues:

condensed chromosomes still scattered or nuclear boundary disappearing → prophase
duplicated chromosomes arranged along one central plane → metaphase

Mitosis is continuous; phase names label dominant visible events rather than pauses between separate processes.

Anaphase: centromere linkage is released and sister chromatids move to opposite poles. Once separated, each chromatid is a daughter chromosome.

Telophase: chromosomes reach the poles and decondense; nuclear envelopes and nucleoli re-form around the two chromosome sets.

Identification cues:

two separating groups, often V-shaped as centromeres lead → anaphase
two groups at opposite ends with new nuclear boundaries → telophase

Because sister chromatids were replicated copies and one moves to each pole, the two daughter nuclei normally contain identical chromosome sets.

Use a fixed observation sequence:

Are individual condensed chromosomes visible?
Are they scattered, aligned at one equator, separating, or already at opposite poles?
Is one nuclear envelope present, absent, or re-forming as two?

Dominant observation	Best stage identification
chromatin diffuse inside an intact nucleus	interphase, not mitosis
condensed chromosomes not yet aligned	prophase
chromosomes aligned at one equator	metaphase
daughter chromosomes moving apart	anaphase
two chromosome groups with re-forming nuclei	telophase

A stained root-tip squash contains many cells in different stages because division is not synchronized. Count only cells whose chromosome evidence is sufficiently clear.

A single still image may lie near a phase boundary. Record the visible cue and acknowledge uncertainty rather than forcing a label from cell outline alone.

DNA replication creates joined sister chromatids → chromosomes condense and attach to the spindle → metaphase alignment checks bipolar attachment → sister chromatids separate → two nuclei re-form → cytokinesis partitions the cytoplasm

Continuity requirement	What supplies it
complete genome in each nucleus	replication followed by equal chromatid separation
controlled chromosome movement	condensation, spindle microtubules and motor proteins
two separate cells	animal cleavage furrow or plant cell plate
suitable daughter-cell contents	equal or functionally unequal cytoplasmic partition

To identify a stage, prioritize chromosome position and nuclear-envelope state. To explain the outcome, connect those observations to what is being separated.

Before meiosis, S phase replicates every chromosome into two sister chromatids. The nucleus is still diploid because both homologues of each pair remain present.

A diploid cell replicates DNA once, separates homologous chromosomes in meiosis I and separates chromatids in meiosis II to form four haploid nuclei.

In meiosis I, homologous maternal and paternal chromosomes separate into different nuclei. Chromosome number is reduced from diploid to haploid, although each chromosome still has two chromatids.

There is no second DNA replication. In meiosis II, sister chromatids separate, producing four haploid nuclei with one chromosome from each homologous pair.

Reduction prevents chromosome number doubling in every generation: haploid gametes fuse at fertilization to restore the diploid number.

A bivalent is a paired set of duplicated homologous chromosomes: one maternal homologue and one paternal homologue, each made of two sister chromatids.

Question	Meiosis I	Meiosis II
what aligns?	bivalents	individual duplicated chromosomes
what separates?	homologous chromosomes	sister chromatids
do centromeres divide?	no	yes
chromosome-number effect	diploid → haploid	remains haploid

Use the object being separated in explanations: homologues move apart in anaphase I; sister chromatids move apart in anaphase II.

Calling both events 'chromosomes separating' hides the reason meiosis I is the reduction division.

A homologous pair can fail to separate in meiosis I, or sister chromatids can fail to separate in meiosis II. This failure is non-disjunction.

Both copies move to one pole while the opposite pole receives none. Later division therefore cannot give every gamete the standard chromosome number.

The affected meiosis produces gametes with an extra chromosome (n + 1) and/or a missing chromosome (n − 1), depending on when the error occurred.

After fusion with a normal haploid gamete, an n + 1 gamete can produce a trisomic zygote; an n − 1 gamete can produce a monosomic zygote.

Non-disjunction can create too many or too few chromosomes. It is not defined only by an extra chromosome.

chromosome 21 non-disjunction during gamete formation → gamete receives two copies of chromosome 21 → fertilization by a normal gamete adds one more copy → zygote has three copies of chromosome 21

The resulting trisomy 21 gives the zygote 47 chromosomes rather than the usual 46 and can cause Down syndrome.

The developmental effects vary among individuals because an extra chromosome changes the dosage of many genes, not just one gene.

Down syndrome is a chromosome-number condition. It is not caused by a point mutation within chromosome 21.

During prophase I, duplicated homologous chromosomes pair closely as a bivalent. Corresponding gene loci align.

Non-sister chromatids break at corresponding positions and rejoin to the other homologue. The visible connection is a chiasma.

Equivalent DNA segments are exchanged, producing recombinant chromatids with new combinations of maternal and paternal alleles.

Crossing over is between non-sister chromatids of homologous chromosomes. It rearranges existing alleles; it does not necessarily create new alleles.

At metaphase I, each bivalent can face either pole independently of the others. The maternal or paternal homologue that enters a gamete is therefore random for each pair.

$2^n$

For humans, $n=23$ , so random orientation alone can produce $2^{23}$ —more than 8 million—chromosome combinations before crossing over is counted.

Random fusion of one genetically varied sperm with one genetically varied egg multiplies the possible allele combinations again.

Crossing over changes allele combinations within chromosomes; random orientation changes which whole maternal and paternal homologues travel together.

Event	What changes	Main consequence
replication before meiosis	each chromosome gains a sister chromatid	DNA prepared for two divisions
meiosis I	homologous chromosomes separate	chromosome number is halved
meiosis II	sister chromatids separate	four haploid products can form
non-disjunction	one required separation fails	aneuploid gametes may form

Variation is layered: crossing over recombines alleles within chromosomes, random orientation assort homologues independently, and random fertilization combines two independently produced gametes.

When explaining any meiotic outcome, name the stage, the chromosome object that should separate, the chromosome number before and after, and whether the result changes number, allele combination or both.

Cell proliferation is an increase in cell number through repeated cell growth and mitotic division. The new cells may remain unspecialized, differentiate or replace cells that were lost.

Early embryo: rapid divisions build cell number before extensive differentiation.
Plant meristems: dividing cells at apical or lateral growth regions supply new plant tissues.
Routine replacement: stem-cell lineages replenish short-lived cells such as epidermal cells.
Wound repair: fibroblasts and other cells proliferate to rebuild tissue and extracellular matrix.

Proliferation describes more cells. Cell enlargement and differentiation can follow, but they are different processes.

After fertilization, repeated mitotic divisions increase cell number from a zygote through two-, four- and eight-cell stages to a blastocyst.

The cell cycle is the repeating sequence in which a cell grows and prepares during interphase, divides its nucleus by mitosis and partitions its cytoplasm by cytokinesis.

G1 growth and biosynthesis → S-phase DNA replication → G2 growth and division preparation → mitosis → cytokinesis → daughter cells enter a new cycle or leave active cycling

A cell is not in mitosis for most of its cycle. Interphase is usually the longest portion, so most cells in a tissue sample are expected to appear in interphase.

A circular cell-cycle diagram orders G1, S and G2 interphase before mitosis and cytokinesis return the lineage to G1.

Interphase stage	Main work	Chromosome state by the end
G1	cell growth, metabolism, protein and organelle production	each chromosome has one chromatid
S	DNA replication	each chromosome has two sister chromatids
G2	further growth, protein synthesis and preparation for spindle formation	replicated chromosomes remain joined

The order matters: the cell first builds capacity, then copies the genome once, then checks and prepares the machinery needed to distribute those copies.

DNA quantity doubles during S phase, but chromosome number does not double because the sister chromatids remain joined at their centromere.

During interphase the cell transcribes genes, synthesizes proteins, grows its cytoplasm, accumulates energy and increases organelles. DNA is dispersed as chromatin and remains accessible for gene expression.

Interphase duration varies with cell fate: rapidly proliferating embryo or meristem cells cycle quickly, many adult cells divide only when signalled, and some differentiated cells remain outside active division for long periods.

A nucleus that looks uniform under a light microscope is not resting. Lack of visible condensed chromosomes is evidence of chromatin state, not metabolic inactivity.

An interphase cell is surrounded by protein synthesis, DNA replication, cell growth and organelle increase.

Cyclin-dependent kinases (CDKs) are present but require particular cyclins to become active. Cyclin concentrations rise and fall, giving the control system time-specific signals.

Cyclin accumulates and binds its CDK → the active complex phosphorylates target proteins → a checkpoint transition can occur once the relevant conditions and threshold are satisfied.

At the G2/M transition, cyclin–CDK activity forms mitosis-promoting factor (MPF), triggering chromosome condensation, nuclear-envelope breakdown and spindle assembly.

Cyclin is then degraded while CDK can be reused. Falling complex activity helps make the transition directional and resets control for a later cycle.

Cyclin level is part of checkpoint control, not the only input. DNA integrity, replication completion, spindle attachment and external signals also influence progression.

Gene class	Normal role	Cancer-promoting change	Analogy
proto-oncogene	stimulates division when an appropriate signal is present	gain-of-function mutation creates an oncogene with excessive or constant activity	accelerator stuck on
tumour-suppressor gene	stops the cycle, repairs damage or promotes apoptosis	loss-of-function mutation removes restraint	brake lost

A mutant Ras oncogene can keep growth-signalling pathways active without the normal extracellular signal. One activated allele may be sufficient to increase signalling.

Loss of p53 function can prevent arrest or apoptosis after DNA damage. Because a remaining functional copy can still supply p53, both copies often need to be lost in the affected cell lineage.

Cancer usually develops through accumulated mutations and clonal selection, not one mutation that instantly creates a fully malignant tumour.

Property	Benign tumour	Malignant tumour
local growth	often slower and bounded	often faster and poorly controlled
invasion	does not invade neighbouring tissue	penetrates and damages neighbouring tissue
metastasis	absent	cells may detach, travel and form secondary tumours

Metastasis requires several steps: cells detach from the primary tumour, enter blood or lymph, survive transport, leave the vessel and establish a secondary tumour elsewhere.

A tumour is an abnormal mass produced by excess cell division. Not every tumour is cancerous; malignant invasion and metastatic capacity define cancerous behaviour.

A local benign tumour is contrasted with a malignant tumour invading neighbouring tissue and with cells spreading through a vessel to form a secondary tumour.

$MI=\frac{M}{T}\times 100\%$

Let M be the number of cells observed in mitosis and T the total number of cells observed. If 10 of 95 visible cells are in mitosis,

$\frac{10}{95}\times 100\%=10.5\%$

A higher mitotic index means a larger fraction of sampled cells was in mitosis at the observation time. It can support comparison of tissue proliferation or response to treatment.

Mitotic index is not a unique cancer diagnosis. It depends on sampling, stage-identification accuracy and how long cells remain in mitosis; replicate fields and other evidence are required.

Growth or repair signal → G1 growth → S-phase genome replication → G2 preparation and checkpoint control → cyclin–CDK activation → mitosis and cytokinesis → daughter cells differentiate, replace tissue or re-enter the cycle

Oncogene activation can increase positive growth signalling, while tumour-suppressor loss can remove arrest, repair or apoptosis. Accumulated changes allow an abnormal clone to proliferate.

Evidence scale	Question it answers
cell-cycle proteins and genes	why is checkpoint control altered?
mitotic index	what fraction of sampled cells is dividing now?
tissue boundary	is the tumour local or invading?
secondary growths	has metastatic spread occurred?

Rapid division alone is not the whole definition of malignancy. A strong explanation connects molecular control failure to clonal growth, tissue invasion and possible metastasis.

1 mark

Which process contributes to growth of a multicellular body?

8 marks

Compare and contrast the processes of mitosis and cytokinesis in animal and plant cells.

1 mark

Daughter cells usually receive equal amounts of cytoplasm as parent cells undergo cytokinesis. Which of the following is an exception?

5 marks

Distinguish between the processes of meiosis and mitosis.

1 mark

Distinguish between the quantity of DNA of the cell at G1 and G2.

1 mark

What occurs in cell division during both mitosis and meiosis?

9 marks

Describe the events that occur during mitosis.

1 mark

The following shows a micrograph.

How many cells are in metaphase?

5 marks

Outline what occurs in cells in the first division of meiosis.

4 marks

Describe how non-disjunction can cause Down syndrome.

7 marks

Explain the stages and processes of meiosis leading to genetic variation.

3 marks

Based on the data, evaluate the evidence for leptin promoting regeneration of liver tissue.

7 marks

Following germination of seeds, plants undergo a rapid increase in the number of cells. Describe stages in the cell cycle that result in this increase of cells.

4 marks

Outline the processes occurring during interphase in the cell cycle.

4 marks

Explain how the cell cycle is controlled.

4 marks

Explain how changes to the cell cycle can result in tumour formation.

1 mark

Which processes occur during the development of secondary tumours?

I. Cytokinesis
II. Metastasis
III. Mitosis

Next Topic

—D2.2 Gene expression [HL only]Read

D2.1 Cell and nuclear division

Learning objectives

Cell Division Extends an Existing Cell Lineage

Animal Cells Pinch In; Plant Cells Build a Cell Plate

Equal Chromosomes Do Not Require Equal Cytoplasm

Mitosis Preserves Chromosome Number; Meiosis Reduces It

Replication Creates Sister Chromatids before Nuclear Division

Condensation and Spindle Forces Make Chromosomes Movable

Mitosis First Condenses Chromosomes and Aligns Their Centromeres

Mitosis Then Separates Sister Chromatids and Rebuilds Nuclei

Identify a Mitotic Stage from Chromosome Evidence, Not Cell Shape

Reconstruct How One Replicated Cell Becomes Two Daughter Cells

One DNA Replication Followed by Two Divisions Produces Haploid Nuclei

Meiosis I Separates Homologues; Meiosis II Separates Chromatids

Non-Disjunction Sends Both Copies to One Pole

Trisomy 21 Usually Begins with a Meiotic Separation Error

Crossing Over Recombines Alleles within Homologous Chromosomes

Random Orientation and Fertilization Multiply Gamete Variety

Track What Separates to Explain Reduction, Error and Variation

Cell Proliferation Repeats Mitosis for Growth and Repair

The Cell Cycle Alternates Preparation with Division

G1 Builds the Cell, S Copies DNA and G2 Prepares Division

Interphase Is Active Even When Chromosomes Are Not Visible

Cyclin–CDK Complexes Turn Cell-Cycle Transitions On

Cancer Risk Rises When Growth Signals Stick On or Checkpoint Brakes Fail

Invasion and Metastasis Distinguish Malignant Tumours

Mitotic Index Estimates the Fraction of Cells Currently Dividing

Connect Normal Proliferation to Cell-Cycle Control and Cancer

Next Topic

Generation of new cells

Cytokinesis exam focus

Equal and unequal cytokinesis

Roles of mitosis and meiosis

DNA replication prerequisite

Shared features

Phases of mitosis

Identification of mitosis phases

Meiosis as reduction division

Down syndrome

Meiosis generates variation

Cell proliferation

Cell cycle phases

Cell growth during interphase

Cell cycle control by cyclins

Mutations in cell cycle genes

Tumour differences