What is inheritance in the context of Edexcel IGCSE Biology?

In Edexcel IGCSE Biology, inheritance refers to the process by which genetic information is passed from parents to offspring. This occurs through the transmission of genes, which are segments of DNA that determine specific traits. Understanding inheritance helps explain how characteristics are passed down through generations.

How do dominant and recessive alleles affect inheritance?

In inheritance, alleles are different forms of a gene. A dominant allele is one that expresses its trait even if only one copy is present, whereas a recessive allele requires two copies to express its trait. For example, if a dominant allele for brown eyes is present, it will mask the effect of a recessive allele for blue eyes, resulting in brown eyes.

What is the role of chromosomes in inheritance?

Chromosomes are structures within cells that contain DNA and genes. In humans, each cell typically contains 23 pairs of chromosomes. During reproduction, chromosomes are passed from parents to offspring, ensuring that genetic information is inherited. This process is crucial for the continuation of genetic traits across generations.

How does Mendel's work relate to modern understanding of inheritance?

Gregor Mendel's experiments with pea plants laid the foundation for modern genetics. He discovered the principles of inheritance, such as the concepts of dominant and recessive traits, and the segregation of alleles. These principles are still used today to understand how traits are inherited in both plants and animals, including humans.

What is a Punnett square and how is it used in studying inheritance?

A Punnett square is a diagram used to predict the outcome of a particular genetic cross. It helps visualize how alleles from each parent can combine in offspring. By using a Punnett square, students can calculate the probability of inheriting specific traits, making it a valuable tool in studying inheritance patterns in Edexcel IGCSE Biology.

Why is "Using 'gene' and 'allele' interchangeably" a common mistake in Inheritance?

Why it happens: Both relate to inheritance; the distinction is subtle. How to avoid it: **Gene = the characteristic** (e.g. gene for tongue-rolling). **Allele = one version of the gene** (e.g. T or t, the dominant or recessive allele for tongue-rolling). Every gene has at least 2 alleles in a population. Source: 4BI1 Examiner Reports 2022-2024

Why is "Forgetting that meiosis halves the chromosome number" a common mistake in Inheritance?

Why it happens: Confusion between mitosis and meiosis. How to avoid it: **Mitosis: chromosome number STAYS THE SAME** (46 → 46 in humans). **Meiosis: chromosome number is HALVED** (46 → 23). This is essential — gametes MUST be haploid so that when they fuse at fertilisation, the DIPLOID number is restored. Source: 4BI1 Examiner Reports 2024

Why is "Saying organisms 'want to' or 'try to' adapt to their environment (Lamarckian thinking)" a common mistake in Inheritance?

Why it happens: Common misconception that evolution is purposeful. How to avoid it: Natural selection is NOT purposeful. Variation arises by RANDOM MUTATION before any selection pressure. The environment then SELECTS for organisms that happen to have favourable alleles. Use phrases like 'mutation produced...', 'individuals with X were more likely to survive', 'allele frequency increased' — NOT 'animals developed', 'bacteria wanted to'. Source: 4BI1 Examiner Reports 2023-2024

Why is "Saying sons inherit X from their father" a common mistake in Inheritance?

Why it happens: Forgetting that the father donates X to daughters and Y to sons. How to avoid it: Father is XY. He passes ONE sex chromosome to each child: X → daughter; Y → son. So **sons inherit Y from their father, X from their mother**. This is why X-linked recessive disorders (haemophilia, colour blindness) tend to affect males — they have only one X. Source: 4BI1 Examiner Reports 2024

Why is "Drawing a Punnett square correctly but not stating the phenotype ratio" a common mistake in Inheritance?

Why it happens: Stopping at the genotypes. How to avoid it: ALWAYS state the phenotype ratio in your final answer (e.g. '3 brown : 1 blue', '1 : 1', '50%'). The mark scheme always reserves a mark for the explicit ratio. Both 'ratio' and 'percentage' are accepted, but be clear. Source: 4BI1 Examiner Reports 2022-2024

Why is "Saying mutations are always harmful" a common mistake in Inheritance?

Why it happens: Headlines focus on harmful mutations (cancer, genetic disease). How to avoid it: MOST mutations are neutral (no effect). SOME are harmful (e.g. sickle-cell anaemia). RARELY a mutation is beneficial (e.g. antibiotic resistance in bacteria, lactase persistence). Beneficial mutations are the RAW MATERIAL of evolution — without them, no natural selection. Source: 4BI1 Examiner Reports 2023

Why is "Saying eye colour is discontinuous variation" a common mistake in Inheritance?

Why it happens: Simplification in textbooks. How to avoid it: Eye colour is actually CONTINUOUS (many shades of brown, hazel, green, blue, grey) — it is polygenic. The classic exam-safe example for DISCONTINUOUS variation is ABO blood group (only A, B, AB, O). For CONTINUOUS: height, body mass, foot length. Source: 4BI1 Examiner Reports 2024

Why is "Saying 'the individual evolves' or 'the bacterium became resistant'" a common mistake in Inheritance?

Why it happens: Misunderstanding of how evolution works. How to avoid it: Individuals do NOT evolve. POPULATIONS evolve. The individual either has the advantageous allele (and survives) or doesn't (and may die). Over generations, the frequency of advantageous alleles increases in the POPULATION → this is evolution. Source: 4BI1 Examiner Reports 2024

Reproduction and InheritanceEdexcel IGCSE Biology (4BI1)

Inheritance

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Inheritance — Pearson Edexcel International GCSE Biology 4BI1 Study Notes (2026 onwards, Spec Issue 4)

DNA structure and the genetic code; genes, alleles, chromosomes; mitosis and meiosis; monohybrid crosses with Punnett squares; codominance (ABO blood groups); sex determination and sex linkage (haemophilia, colour blindness); continuous vs discontinuous variation; mutations; and the Darwin-Wallace theory of natural selection (Paper 2). Covers spec 3.17-3.40P.

At a glance

DNA = double helix; bases pair A-T, C-G. Gene = section of DNA coding for a protein.
Allele = version of a gene; homozygous = same alleles; heterozygous = different alleles.
Chromosomes: humans have 23 PAIRS (46). 22 autosomes + 1 sex pair (XX female / XY male).
Mitosis = 2 identical daughter cells, diploid (growth/repair).
Meiosis = 4 different daughter cells, HAPLOID (gametes).
Codominance: BOTH alleles expressed (e.g. blood group AB).
Sex linkage: X-linked recessive disorders mainly affect males (XY).
Continuous = range (height, polygenic); discontinuous = distinct categories (blood group, monogenic).
Mutation = random change in DNA base sequence. Most neutral, some harmful, rarely beneficial.
Natural selection (Paper 2): variation → selection → survival → reproduction → allele frequency rises.

What you’ll learn

Mapped to the Cambridge IGCSE 4BI1 syllabus (2026 onwards).

3.17 — Understand that the nucleus contains chromosomes on which genes are located.
3.18 — Understand that a gene is a section of DNA. DNA is a double helix; bases pair A-T and C-G.
3.19 — Understand the meaning of: genotype, phenotype, allele (dominant + recessive), homozygous, heterozygous.
3.20 — Understand that an organism's body cells are diploid (2 of each chromosome); gametes are haploid (1 of each).
3.21 — Understand the mitotic cell cycle: parent cell → 2 genetically identical daughter cells with same chromosome number.
3.22 — Understand the role of mitosis in growth, repair and asexual reproduction.
3.23 — Understand the role of meiosis in producing gametes that are genetically different and have half the chromosome number.
3.24 — Understand the relationship between mitosis, meiosis, fertilisation and the diploid/haploid life cycle.
3.25 — Predict the outcome of monohybrid crosses involving dominant and recessive alleles, using genetic diagrams and Punnett squares.
3.26 — Calculate and predict genotype + phenotype ratios in F1 and F2 generations.
3.27 — Use family pedigrees to deduce genotypes.
3.28 — Understand the concept of codominance and recall an example (e.g. ABO blood groups).
3.29 — Understand how sex is determined in humans by the X and Y chromosomes.
3.30 — Understand sex linkage and predict outcomes of sex-linked crosses (e.g. haemophilia, colour blindness).
3.31 — Recall that variation may be discontinuous (controlled by a single gene) or continuous (controlled by many genes; influenced by environment).
3.32 — Understand that variation arises through mutation, meiosis and fertilisation.
3.33 — Understand that mutations are random, can occur naturally, and can be increased by ionising radiation and chemical mutagens.
3.34 — Understand that most mutations are neutral, some are harmful, rarely beneficial.
3.35-3.40P — (Paper 2) Understand the theory of evolution by natural selection: variation, selection pressure, survival of the fittest, reproduction, allele frequency. Examples: peppered moth (industrial melanism), antibiotic resistance in bacteria, warfarin resistance in rats.

DNA, genes and chromosomes (spec 3.17-3.20)

DNA → genes → chromosomes → proteins. Hierarchical organisation of the genetic code.

DNA structure (spec 3.18):

DNA = deoxyribonucleic acid.
Made of two strands of nucleotides arranged in a DOUBLE HELIX.
Each nucleotide has: a sugar (deoxyribose), a phosphate group, and a NITROGENOUS BASE.
Four bases: A (adenine), T (thymine), C (cytosine), G (guanine).
The strands are held together by base pairing: A always pairs with T; C always pairs with G (complementary base pairing).

Gene = section of DNA (spec 3.18). A gene is a length of DNA that codes for a specific PROTEIN (or polypeptide). The sequence of bases along the gene is read in triplets (codons) — each triplet codes for one amino acid. The chain of amino acids folds into a functional protein.

Examples of proteins encoded by genes:

Enzymes — amylase, lactase, lipase.
Structural proteins — keratin (hair, nails), collagen.
Hormones — insulin, oestrogen (insulin is a protein; steroid hormones are made by protein enzymes).
Antibodies — fight pathogens.

Allele (spec 3.19). An allele is a VERSION of a gene. For example, the gene for tongue-rolling has two alleles in the human population: T (dominant) and t (recessive). Different alleles produce slightly different proteins, leading to different phenotypes.

Chromosome (spec 3.17). A chromosome is a long thread of DNA wound around proteins (histones), found in the nucleus. Each chromosome carries HUNDREDS to THOUSANDS of genes.

Human chromosomes:

46 chromosomes in each diploid body cell.
Arranged as 23 PAIRS — one chromosome from each pair came from the mother, the other from the father.
22 pairs are autosomes (non-sex chromosomes), numbered 1-22.
1 pair is the sex chromosomes — XX in females, XY in males.

Genotype vs phenotype (spec 3.19):

Genotype = the alleles you carry (e.g. Tt). Written with letters (capitals = dominant, lowercase = recessive).
Phenotype = the observable characteristic that results (e.g. tongue-roller). Determined by genotype AND sometimes environment.

Homozygous vs heterozygous (spec 3.19):

Homozygous = TWO SAME alleles (e.g. TT or tt). Called 'pure-breeding'.
Heterozygous = TWO DIFFERENT alleles (e.g. Tt). Often called a 'carrier' when one allele is a recessive disease allele.

Haploid vs diploid (spec 3.20):

Diploid (2n) = TWO of each chromosome (e.g. 46 in humans). Body cells.
Haploid (n) = ONE of each chromosome (e.g. 23 in humans). Gametes only.

DNA is a double helix; bases A-T, C-G.
Gene = section of DNA coding for a protein.
Allele = version of a gene.
Humans: 23 pairs of chromosomes (46 total), 22 autosomes + 1 sex pair.
Homozygous = 2 same alleles; heterozygous = 2 different alleles.

See the full worked example for inheritance →

Mitosis and meiosis (spec 3.21-3.24)

Mitosis: 2 identical diploid cells (growth/repair). Meiosis: 4 different haploid cells (gametes).

Two types of nuclear cell division with very different roles.

MITOSIS (spec 3.21-3.22).

Mitosis produces TWO daughter cells GENETICALLY IDENTICAL to the parent cell, with the SAME chromosome number.

Number of daughter cells: 2.
Number of divisions: 1.
Chromosome number: stays the same (diploid → diploid; 46 → 46).
Genetic identity: daughter cells are IDENTICAL to parent and each other.
Purpose: GROWTH (embryo to adult), REPAIR (wound healing), REPLACEMENT (e.g. skin cells), ASEXUAL REPRODUCTION (bacteria, strawberry runners).

Stages (briefly):

Prophase: chromosomes condense and become visible as two sister chromatids.
Metaphase: chromosomes line up across the middle of the cell.
Anaphase: sister chromatids are pulled apart to opposite ends.
Telophase: new nuclear envelopes form around the two sets; cell divides (cytokinesis).

MEIOSIS (spec 3.23-3.24).

Meiosis produces FOUR daughter cells (gametes) that are GENETICALLY DIFFERENT, with HALF the chromosome number.

Number of daughter cells: 4.
Number of divisions: 2 (Meiosis I + Meiosis II).
Chromosome number: HALVED (diploid → haploid; 46 → 23).
Genetic identity: daughter cells are GENETICALLY DIFFERENT from parent and each other.
Purpose: PRODUCTION OF GAMETES (sperm in testes, eggs in ovaries).

How meiosis creates variation:

Crossing over — during Meiosis I, homologous chromosomes pair up and EXCHANGE sections of DNA. This shuffles alleles between maternal and paternal chromosomes.
Independent assortment — when the homologous pairs separate, each daughter cell gets a RANDOM combination of maternal and paternal chromosomes. For 23 pairs, that's 2^23 ≈ 8 million combinations.
Random fertilisation — combined with random meeting of sperm and egg, the genetic possibilities are essentially infinite.

The life cycle (spec 3.24):

Body cell (diploid, 2n=46) → MITOSIS → 2 body cells (2n=46) → growth and repair. Body cell (2n=46) → MEIOSIS → 4 gametes (n=23) → SEX with another gamete → FERTILISATION → zygote (2n=46) → MITOSIS → body of new organism.

The diploid-haploid alternation is the core of sexual reproduction:

Meiosis HALVES the chromosome number (so gametes are haploid).
Fertilisation RESTORES the chromosome number (so zygote is diploid).
Mitosis then grows the diploid zygote into a multicellular adult.

Mitosis: 1 → 2 identical diploid cells. Growth, repair, asexual.
Meiosis: 1 → 4 different haploid cells. Gamete production.
Variation in meiosis: crossing over + independent assortment.
Diploid (46) → meiosis → haploid (23) → fertilisation → diploid (46).

See the full worked example for inheritance →

Monohybrid crosses and Punnett squares (spec 3.25-3.27)

Predict offspring genotypes and phenotypes using a Punnett square.

A genetic cross is a way to predict the genotypes and phenotypes of offspring from given parents.

Steps to solve a monohybrid cross:

Define the alleles. State which allele is dominant (capital) and which is recessive (lowercase). E.g. T = tongue-roller (dominant), t = non-roller (recessive).
State parental genotypes. Use the information given (or work it out from phenotypes).
State the gametes that each parent can produce (use rings or boxes).
Draw a Punnett square crossing the gametes.
State the offspring genotypes in each cell of the square.
State the phenotypes corresponding to each genotype.
State the ratio of phenotypes (or percentage / probability).

Example: heterozygous × homozygous recessive (test cross).

Cross: Tt × tt

	t (parent 2)	t (parent 2)
T (parent 1)	Tt	Tt
t (parent 1)	tt	tt

Phenotypes: 2 tongue-rollers (Tt) : 2 non-rollers (tt) = 1 : 1.

Example: heterozygous × heterozygous.

Cross: Tt × Tt

	T	t
T	TT	Tt
t	Tt	tt

Offspring genotypes: 1 TT : 2 Tt : 1 tt. Phenotype ratio: 3 tongue-rollers (TT + 2 Tt) : 1 non-roller (tt) = 3 : 1.

This is the classic 3 : 1 Mendelian ratio for a heterozygous cross.

Example: homozygous dominant × homozygous recessive.

Cross: TT × tt → all offspring are Tt → all tongue-rollers.

Pedigrees (spec 3.27):

A pedigree (family tree) shows phenotypes across generations. Squares = males, circles = females. Filled = affected; empty = unaffected. Horizontal line between two parents; vertical line down to children.

Use pedigree logic to deduce genotypes:

If both parents are unaffected but a child is affected → both parents must be heterozygous carriers (Aa × Aa → 1/4 aa affected).
If an affected father has an unaffected daughter → the daughter must be a heterozygote (if it's a dominant trait) or has inherited the dominant allele from her mother (if recessive).

Tt × tt → 1:1 phenotype ratio (test cross).
Tt × Tt → 3:1 phenotype ratio (classic Mendelian).
TT × tt → all Tt (all show dominant phenotype).
ALWAYS state the phenotype ratio in your answer.

See the full worked example for inheritance →

Codominance and sex determination (spec 3.28-3.30)

Codominance: both alleles expressed (e.g. AB blood). Sex linkage: X-linked alleles mainly affect males.

Codominance (spec 3.28).

Definition: when TWO alleles are BOTH expressed in the heterozygous genotype — neither allele is dominant over the other.

Classic example: ABO blood groups.

Three alleles: I^A, I^B, i.
I^A and I^B are CODOMINANT (both expressed when present together).
i is recessive to both.
Genotypes and phenotypes:

Genotype	Phenotype (blood group)	Antigens on red blood cells
I^A I^A or I^A i	A	A antigens only
I^B I^B or I^B i	B	B antigens only
I^A I^B	AB	BOTH A and B antigens (codominance!)
ii	O	No antigens

The heterozygous I^A I^B individual makes BOTH the A antigen AND the B antigen — that is the codominance.

Example cross. A blood group AB parent (I^A I^B) × blood group O parent (ii):

	I^A	I^B
i	I^A i (A)	I^B i (B)
i	I^A i (A)	I^B i (B)

Offspring: 50% blood group A, 50% blood group B. NEVER AB or O from this cross.

Sex determination (spec 3.29).

Females: XX (two X chromosomes; produce only X gametes).
Males: XY (one X, one Y; produce X gametes or Y gametes 50/50).
A baby's sex is determined by the FATHER (whether his sperm contained X or Y).
The SRY gene on the Y chromosome triggers male development; without it the embryo develops as female.
Female × male cross:

	X (mum)	X (mum)
X (dad)	XX (girl)	XX (girl)
Y (dad)	XY (boy)	XY (boy)

Ratio: 1 boy : 1 girl, 50:50.

Sex-linked inheritance (spec 3.30).

A 'sex-linked' gene is one carried on the X chromosome (the Y chromosome carries very few genes). The Y has no equivalent allele.

Why males are more affected:

Males (XY) have only ONE X → any X-linked recessive allele they carry is automatically expressed (they are HEMIZYGOUS, not homozygous).
Females (XX) need BOTH X chromosomes to carry the recessive allele to be affected; heterozygotes are CARRIERS.

Common X-linked recessive disorders:

Haemophilia — blood-clotting factor missing; bleeding doesn't stop.
Red-green colour blindness — cannot distinguish red and green hues.
Duchenne muscular dystrophy — muscle weakening.

Symbols. Write X^H = dominant healthy allele; X^h = recessive disease allele. (Superscript H/h after X.)

Inheritance pattern for haemophilia:

Mother	Father	Possible children
X^H X^H (normal)	X^H Y (normal)	All normal
X^H X^h (carrier)	X^H Y (normal)	1/4 carrier daughters, 1/4 normal daughters, 1/4 normal sons, 1/4 affected sons
X^H X^H (normal)	X^h Y (affected)	1/2 carrier daughters, 1/2 normal sons
X^H X^h (carrier)	X^h Y (affected)	1/4 carrier daughters, 1/4 affected daughters, 1/4 normal sons, 1/4 affected sons

Key facts:

Fathers pass X^h to ALL daughters; pass Y to ALL sons.
Carrier mothers pass X^h to ~50% of all children.
Sons NEVER inherit X-linked recessives from their fathers (they get Y from father).

Codominance: both alleles expressed (heterozygote shows BOTH phenotypes).
ABO: I^A I^B → blood group AB (both A and B antigens).
XX = female, XY = male. Father determines sex.
Sex-linked recessives mainly affect males (XY — only one X).
Father passes X to daughters, Y to sons.

See the full worked example for inheritance →

Variation and mutation (spec 3.31-3.34)

Continuous vs discontinuous variation. Mutations are random changes in DNA — most neutral, rarely beneficial.

Types of variation (spec 3.31):

Feature	Continuous	Discontinuous
Pattern	Range of values, all intermediates possible	Distinct categories, no intermediates
Distribution	Normal distribution (bell curve)	Frequency in discrete groups (bar chart)
Type of data	Quantitative (measurements)	Qualitative (categories)
Genetic control	POLYGENIC (many genes)	Monogenic (one or few genes)
Environmental influence	Significant	Minimal
Examples (humans)	Height, mass, foot length	ABO blood group, sex, tongue-rolling

Why continuous variation has a normal distribution: because many genes contribute, each with small effect, the outcomes cluster around an average. Combined with environmental effects (e.g. diet on height), the result is a smooth bell-curve distribution.

Sources of variation (spec 3.32):

Mutation — new alleles created.
Meiosis — crossing over + independent assortment shuffle existing alleles.
Random fertilisation — any sperm can meet any egg.
Environment — diet, exercise, climate affect the phenotype.

Mutations (spec 3.33).

Definition: a random, spontaneous change in the BASE SEQUENCE of DNA.

Types of mutation:

Point mutation — single base substituted.
Insertion / deletion — extra base added or removed (often causes frameshift).
Chromosomal — larger sections deleted, duplicated, inverted or translocated.

Effects of mutations (spec 3.34):

NEUTRAL (most common). Mutation occurs in non-coding DNA, or the new triplet still codes for the same amino acid (degenerate code) → no change in protein → no effect on phenotype.
HARMFUL. Mutation changes the amino acid sequence → produces a non-functional or abnormal protein → may cause disease.
- Sickle-cell anaemia — single base change in haemoglobin gene → abnormal HbS.
- Cystic fibrosis — deletion of 3 bases in CFTR gene → faulty chloride channel.
- Cancer — mutations in genes controlling cell division.
BENEFICIAL (rare). Mutation produces a protein that gives an advantage.
- Antibiotic resistance in bacteria.
- Lactase persistence in adult humans.
- Warfarin resistance in rats.
- These are the RAW MATERIAL of natural selection.

Factors that INCREASE mutation rate:

Ionising radiation — X-rays, gamma rays, UV light. The high-energy photons damage DNA bases and break DNA strands.
Mutagenic chemicals — tobacco smoke (benzo[a]pyrene), asbestos, formaldehyde, certain dyes.
Heat — destabilises the DNA double helix.
Some viruses — insert their DNA into the host genome.
Errors during DNA replication — DNA polymerase makes mistakes (~1 in 10^9 bases).

Continuous (height) — polygenic + environmental; bell curve.
Discontinuous (blood group) — monogenic; distinct categories.
Mutation = random change in DNA base sequence.
Most mutations neutral; some harmful; rarely beneficial.
Mutation rate increased by ionising radiation + chemical mutagens.

See the full worked example for inheritance →

Natural selection — Darwin & Wallace (spec 3.35-3.40P, Paper 2)

Variation → selection pressure → survival of the fittest → reproduction → allele frequency rises.

This section is mostly BOLD-P content — examined in Paper 2 only (4BI1/2B).

The four steps of natural selection (memorise the sequence):

VARIATION exists in the population. Random mutations and genetic shuffling (meiosis + fertilisation) produce individuals with different alleles.
SELECTION PRESSURE. The environment imposes a selection pressure — e.g. a predator, a disease, climate change, scarce food, or an antibiotic. Some alleles give an ADVANTAGE in coping with this pressure.
SURVIVAL OF THE FITTEST. Individuals with the advantageous allele are more likely to SURVIVE the selection pressure. Individuals without it are more likely to die before reproducing.
REPRODUCTION. The survivors REPRODUCE and pass on their advantageous allele to their offspring. Over many generations, the FREQUENCY of the advantageous allele INCREASES in the population — the population is said to have ADAPTED or EVOLVED.

This is the only known scientific explanation of evolution. It explains the origin of all species from common ancestors.

Three classic examples (spec 3.40P):

Example 1 — Peppered moth (industrial melanism).

Two forms of the peppered moth (Biston betularia): a pale 'typica' form and a dark 'carbonaria' form.
Before the Industrial Revolution: tree bark was light → pale moths were CAMOUFLAGED, dark moths were visible to bird predators. Pale form dominated.
During the Industrial Revolution: soot from factories darkened the tree bark → pale moths now visible, dark moths CAMOUFLAGED. Dark form quickly became most common in industrial areas.
After clean-air laws (1950s onwards): bark lighter again → pale form returning.
This is directional natural selection in action — and it happened over decades, observable in real time.

Example 2 — Antibiotic resistance in bacteria.

Bacterial populations show variation — some have a mutation conferring antibiotic resistance (e.g. an enzyme that breaks down penicillin).
When the antibiotic is used (the selection pressure), most non-resistant bacteria die.
The few resistant survivors reproduce (very rapidly, every 20-30 min) and pass on the resistance allele.
Over generations, the population becomes mostly resistant → the antibiotic stops working.
MRSA (Methicillin-Resistant Staphylococcus Aureus) is a famous example. Resistant TB and gonorrhoea are increasingly serious.
This is why doctors warn against overusing antibiotics and not finishing courses.

Example 3 — Warfarin resistance in rats.

Warfarin is a poison used to control rats — it interferes with blood clotting.
Originally very effective; killed most rats.
A mutation in the VKORC1 gene gave some rats resistance to warfarin.
These resistant rats survived poison treatments and reproduced.
Over decades, resistant rats spread → warfarin became less effective in many areas.

The general lesson. Natural selection requires:

Heritable variation (different alleles, passed on to offspring).
A selection pressure (something that affects survival).
Differential reproduction (those with advantageous alleles have more offspring).

Without any one of these, no evolution by natural selection.

Common misconception to AVOID. Natural selection is NOT 'organisms adapting because they want to' — it is a STATISTICAL process. The variation exists FIRST (random mutation), then selection sorts it. Organisms do not 'try to' evolve; they either have the right alleles or they don't.

Steps: variation → selection pressure → survival → reproduction → allele frequency rises.
Mutation is the ORIGINAL source of new variation.
Examples: peppered moth, antibiotic resistance, warfarin resistance in rats.
AVOID Lamarckian thinking — organisms don't 'try' to adapt.

See the full worked example for inheritance →

Quick recap

DNA = double helix; bases A-T, C-G. Gene = section of DNA → protein. Allele = version of a gene.
Humans: 23 pairs of chromosomes (46). 22 autosomes + 1 sex pair (XX female, XY male).
Mitosis: 2 identical diploid cells (growth, repair).
Meiosis: 4 different haploid cells (gametes). Variation from crossing over + independent assortment.
Genetic crosses: Tt × Tt → 3:1 phenotype ratio. Tt × tt → 1:1.
Codominance: both alleles expressed (e.g. ABO blood group AB).
Sex linkage: X-linked recessives mostly affect males (XY).
Continuous (height) — polygenic; discontinuous (blood group) — monogenic.
Mutation = random DNA base sequence change. Most neutral; some harmful; rarely beneficial.
Natural selection: variation → selection pressure → survival → reproduction → allele frequency rises.

How it’s examined

Inheritance is examined every series — typically 10-15 marks per paper. Paper 1 (4BI1/1B): definitions (gene, allele, genotype, phenotype, homozygous, heterozygous); monohybrid Punnett squares (Tt × Tt = 3:1; Tt × tt = 1:1); structure of DNA + chromosomes; comparison of mitosis vs meiosis; named examples of continuous + discontinuous variation. Paper 2 (4BI1/2B): codominance Punnett squares (ABO blood groups); sex-linked crosses (haemophilia, colour blindness); full description of natural selection with named example (peppered moth, antibiotic resistance); explanation of mutations and their causes. Examiner reports highlight repeating errors: (1) confusing 'gene' and 'allele'; (2) Lamarckian thinking ('bacteria became resistant'); (3) forgetting that sons inherit Y (not X) from their father; (4) failing to state phenotype ratio in Punnett-square answers; (5) saying 'eye colour is discontinuous' (use ABO blood group instead). Use X^superscript notation for sex-linked alleles, and always end with a phenotype ratio (e.g. 1:1, 3:1).

Sources: Pearson Edexcel International GCSE Biology 4BI1 specification — Issue 4, September 2024 (valid for 2026 onwards); Pearson Edexcel 4BI1 Examiner Reports 2022-2024; 4BI1/1B May/Jun 2024 question paper and mark scheme; 4BI1/1B January 2024 question paper and mark scheme; 4BI1/2B May/Jun 2024 question paper and mark scheme; 4BI1/2B January 2024 question paper and mark scheme. Last reviewed 2026-05-12.

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Step-by-step worked examples — Inheritance

Step-by-step solutions to past-paper-style questions on inheritance, written exactly the way a tutor would explain them at the board.

1Distinguish between mitosis and meiosis (5 marks, Paper 1)
Core• Adapted from 4BI1/1B May/Jun 2024 Q7(a)• mitosis, meiosis, cell division, spec-3.22
Question
State FIVE differences between mitosis and meiosis. (5 marks)
Step-by-step solution
1. Step 1
  Number of daughter cells (B1). Mitosis = 2 daughter cells per division. Meiosis = 4 daughter cells per division (after two rounds).
2. Step 2
  Chromosome number (B1). Mitosis = chromosome number STAYS THE SAME (diploid → diploid; 46 → 46 in humans). Meiosis = chromosome number HALVED (diploid → haploid; 46 → 23 in humans).
3. Step 3
  Genetic identity (B1). Mitosis = daughter cells are genetically IDENTICAL to the parent cell (and to each other). Meiosis = daughter cells are genetically DIFFERENT from the parent cell and from each other (because of crossing over + independent assortment).
4. Step 4
  Purpose (B1). Mitosis = growth, repair, replacement of cells, asexual reproduction. Meiosis = production of GAMETES for sexual reproduction.
5. Step 5
  Number of divisions (B1). Mitosis = ONE division (one round of separation). Meiosis = TWO divisions (Meiosis I + Meiosis II), resulting in four cells.
Answer
(1) Mitosis: 2 daughter cells; meiosis: 4. (2) Mitosis: chromosome number same (diploid); meiosis: halved (haploid). (3) Mitosis: daughters identical to parent; meiosis: genetically different. (4) Mitosis: growth/repair/asexual; meiosis: gamete production. (5) Mitosis: one division; meiosis: two divisions.
Examiner tip
Mark scheme awards B1 per CLEAR comparison (both sides of the pair must be given). Examiner reports flag candidates who write 'mitosis = 2, meiosis = 4' without mentioning what these numbers refer to (daughter cells). Use the words DIPLOID and HAPLOID — they're mark-scheme keywords.
2Punnett square for a monohybrid cross (5 marks, Paper 1)
Core• Adapted from 4BI1/1B January 2024 Q7• genetic cross, Punnett square, monohybrid, spec-3.27
Question
In humans, the ability to roll the tongue is determined by a dominant allele T. Inability to roll the tongue is determined by the recessive allele t. A heterozygous tongue-roller (Tt) and a non-roller (tt) have a child. Use a Punnett square to predict the genotypes and phenotypes of the possible offspring, and state the expected ratio. (5 marks)
Step-by-step solution
1. Step 1
  State the parental genotypes (B1). Mother (heterozygous tongue-roller) = Tt. Father (non-roller) = tt. Tongue-roller = phenotype with at least one T. Non-roller = tt (homozygous recessive).
2. Step 2
  Identify the gametes (B1). Tt parent produces gametes: T or t (50% : 50%). tt parent produces gametes: t or t (all t).
3. Step 3
  Draw the Punnett square (M1).
  
  t (father) t (father)
  T (mother) Tt Tt
  t (mother) tt tt
  
  The 4 possible offspring genotypes are: Tt, Tt, tt, tt.
4. Step 4
  State genotypes and phenotypes (A1, depends on M1). Two children would be Tt = tongue-rollers (heterozygous, dominant T expressed). Two children would be tt = non-rollers (homozygous recessive).
5. Step 5
  State the expected ratio (B1). Phenotype ratio: 2 tongue-rollers : 2 non-rollers = 1 : 1. (Or 50% chance of either.) Genotype ratio: 1 Tt : 1 tt.
Answer
Parents Tt × tt. Gametes: T, t × t. Punnett: Tt, Tt, tt, tt. Phenotypes: 2 tongue-rollers (Tt) + 2 non-rollers (tt). Ratio 1 : 1 (50% chance of tongue-rolling).
Examiner tip
Mark scheme: B1 parental genotypes; B1 gametes; M1 correct Punnett square; A1 genotypes of offspring; B1 phenotype ratio. The ratio MUST be stated explicitly. Examiner reports note that candidates who write only the genotypes without stating phenotype ratio lose the final mark. Always end with the phenotype ratio in your answer.
3Sex linkage — haemophilia inheritance (5 marks, Paper 2)
Extended• Adapted from 4BI1/2B May/Jun 2024 Q7(b)• sex linkage, haemophilia, Paper 2, spec-3.30
Question
Haemophilia is a sex-linked recessive disorder caused by an allele on the X chromosome. A boy has haemophilia. His father does not have haemophilia. (a) Explain why the boy cannot have inherited the haemophilia allele from his father. (b) State the genotype of his mother. (5 marks)
Step-by-step solution
1. Step 1
  Sex chromosomes and the haemophilia allele (B1). Females are XX, males are XY. Haemophilia is caused by a recessive allele (X^h) on the X chromosome. The Y chromosome does not carry a corresponding allele.
2. Step 2
  Sons inherit Y from their father (B1). A father passes his Y chromosome to his sons (and his X to his daughters). So the son's X chromosome MUST come from his mother, not his father.
3. Step 3
  The father's X chromosome went to his daughters, not his sons (B1). Even if the father carried X^h, he could not pass it to a son — because sons get Y from the father, NOT X. (In this question, the father doesn't have haemophilia anyway, but the principle stands.)
4. Step 4
  Mother is a CARRIER (B1). For the son to have haemophilia (genotype X^h Y), he must have inherited X^h from his mother. Since the mother does NOT have haemophilia (only X^H X^h is asked here), her genotype must be X^H X^h — she is a heterozygous CARRIER.
5. Step 5
  Explanation of the mother's phenotype (B1). X^H is dominant over X^h. With genotype X^H X^h, the mother does not have haemophilia (the dominant healthy allele is expressed). But she has a 50% chance of passing X^h to each child. If she passes X^h to a son (who gets Y from his father), he will have haemophilia.
Answer
(a) Haemophilia allele is on the X chromosome. Sons inherit Y (not X) from their father, so the son cannot have inherited the allele from his father. (b) Mother must be a heterozygous carrier: X^H X^h. She is phenotypically normal (X^H is dominant) but passes X^h to ~50% of her children. Her son inheriting X^h + father's Y → X^h Y → haemophilia.
Examiner tip
Paper 2 mark scheme: B1 X-linked allele on X chromosome; B1 sons inherit Y from father, X from mother; B1 mother must be carrier (X^H X^h); B1 explanation that X^H is dominant over X^h. Examiner reports stress the symbols: write the alleles as superscripts on X (X^H, X^h), NOT as separate letters H and h. Be precise about why fathers can't pass X-linked recessives to sons.
4Natural selection — antibiotic resistance in bacteria (6 marks, Paper 2)
Extended• Adapted from 4BI1/2B January 2024 Q7(c)• natural selection, evolution, antibiotic resistance, Paper 2, spec-3.40P
Question
Antibiotics are used to kill bacteria, but some populations of bacteria have evolved resistance. Describe how Darwin's theory of natural selection explains the spread of antibiotic resistance in a bacterial population. (6 marks)
Step-by-step solution
1. Step 1
  Variation exists in the bacterial population (M1). A bacterial population shows genetic variation — random MUTATIONS in DNA produce occasional bacteria with a resistance allele.
2. Step 2
  Antibiotic is the SELECTION PRESSURE (M1). When the antibiotic is used (e.g. patient takes a course of antibiotics), most non-resistant bacteria are killed. The resistance allele is now a HUGE survival advantage.
3. Step 3
  Resistant bacteria SURVIVE (A1, depends on M1). The few bacteria that carry the resistance allele are NOT killed by the antibiotic → they survive while non-resistant bacteria die.
4. Step 4
  Resistant bacteria REPRODUCE (A1, depends on M1). The surviving resistant bacteria reproduce (binary fission, very rapidly — every 20-30 min). They pass the resistance allele to their offspring.
5. Step 5
  Allele frequency rises (B1). Over many generations, the proportion of bacteria with the resistance allele INCREASES → the whole population eventually becomes resistant.
6. Step 6
  MRSA / global health relevance (B1). This is why the antibiotic is now ineffective — and why doctors warn against overuse / not finishing courses of antibiotics. Examples include MRSA (Methicillin-Resistant Staphylococcus Aureus) and resistant tuberculosis.
Answer
Genetic VARIATION in the bacterial population — mutation produces resistance allele. 2. Antibiotic = SELECTION PRESSURE — kills non-resistant bacteria. 3. Resistant bacteria SURVIVE. 4. They REPRODUCE and pass on the resistance allele. 5. Frequency of the resistance allele INCREASES in the population. 6. Result: whole population becomes resistant; antibiotic stops working. Examples: MRSA, resistant TB.
Examiner tip
Paper 2 mark scheme awards the 4 'steps' of natural selection: variation (1) → selection pressure (1) → survival of fittest (1) → reproduction → allele frequency rises (1), with up to 2 extra marks for naming the mutation as the source of variation and giving a named example (MRSA). Examiner reports stress that candidates must use the keyword 'MUTATION' as the source of the resistance allele — saying bacteria 'wanted to become resistant' or 'developed resistance' suggests a Lamarckian misunderstanding.
5Continuous vs discontinuous variation (4 marks, Paper 1)
Core• Adapted from 4BI1/1B January 2024 Q5(b)• variation, spec-3.33, spec-3.34
Question
Distinguish between continuous and discontinuous variation, giving a named human example of each. (4 marks)
Step-by-step solution
1. Step 1
  Continuous variation — definition (B1). Differences in a characteristic where there is a RANGE of values between two extremes, with all intermediate values possible. Plotted as a normal distribution (bell curve). Usually QUANTITATIVE.
2. Step 2
  Continuous example (B1). Height in humans — values range continuously from very short to very tall, with most people clustered around the mean. Other examples: body mass, foot length, hand span.
3. Step 3
  Discontinuous variation — definition (B1). Differences in a characteristic where there are DISTINCT, SEPARATE categories with no intermediate values. Plotted as a bar chart (frequency for each category). Usually QUALITATIVE.
4. Step 4
  Discontinuous example + cause (B1). ABO blood group in humans — only 4 possible values (A, B, AB, O); no intermediates. Other examples: tongue-rolling ability, ear-lobe attachment, sex. Why the difference? Continuous traits are usually POLYGENIC (controlled by many genes) and influenced by ENVIRONMENT (e.g. diet affects height). Discontinuous traits are usually MONOGENIC (one or few genes) with little/no environmental influence.
Answer
Continuous = range of values, all intermediates possible, normal distribution, quantitative. Example: height (polygenic + environmental influence). Discontinuous = distinct separate categories, no intermediates, bar chart, qualitative. Example: ABO blood group (monogenic, little environmental influence).
Examiner tip
Mark scheme: B1 definition of continuous; B1 example with reason for continuous variation; B1 definition of discontinuous; B1 example with reason. Examiner reports flag candidates who say 'eye colour is discontinuous' — actually it's continuous because many shades exist (polygenic). Stick to ABO blood group for safety. The key keywords are 'range' (continuous) vs 'distinct categories' (discontinuous).

	t (father)	t (father)
T (mother)	Tt	Tt
t (mother)	tt	tt

Model Answers — Inheritance

High-scoring sample answers for inheritance on the Pearson Edexcel IGCSE 4BI1 paper, with examiner-style notes mapping each response to the mark scheme and assessment objectives.

Question
Adapted from 4BI1/2B May/Jun 2024 Q7(a)6 marks
Explain the relationship between DNA, genes, chromosomes and the proteins made by a cell. (6 marks)
Model answer
DNA — the molecule (B1). DNA (deoxyribonucleic acid) is a long, double-stranded molecule shaped as a DOUBLE HELIX. The two strands are linked by complementary base pairs: A–T (adenine–thymine) and C–G (cytosine–guanine).

Genes — sections of DNA (B1). A GENE is a section of DNA that codes for a specific PROTEIN (or polypeptide). The sequence of bases along the gene specifies the sequence of AMINO ACIDS in the protein. The 'code' is read in triplets — each set of three bases (a CODON) codes for one amino acid.

Chromosomes — packaged DNA (B1). Chromosomes are long, thread-like structures in the nucleus, made of DNA wound around proteins. Each chromosome contains MANY genes. Humans have 23 PAIRS of chromosomes (46 total) in every diploid body cell:

22 pairs of autosomes (numbered 1-22).

1 pair of sex chromosomes (XX in females, XY in males).

Alleles — different versions of a gene (B1). An ALLELE is a different version of the same gene — e.g. the gene for blood group has alleles I^A, I^B and i. Alleles can be DOMINANT (expressed when present) or RECESSIVE (only expressed when homozygous).

From gene to protein (B1). The gene's DNA is transcribed into mRNA, which is then translated at a ribosome → the chain of amino acids folds into a specific PROTEIN. Examples of proteins coded by genes: enzymes (amylase), structural proteins (keratin, collagen), hormones (insulin, oestrogen).

Hierarchy summary (B1).

Cell → contains nucleus → contains chromosomes → made of DNA → contains genes → code for proteins.

A SINGLE chromosome carries hundreds-thousands of genes; a gene is a small section of one chromosome.
Why this scores
Mark scheme: B1 DNA structure (double helix, base pairs); B1 gene = section of DNA coding for a protein; B1 chromosome = many genes; B1 humans have 23 pairs; B1 alleles = versions of a gene; B1 protein function example. Examiner reports note that candidates often confuse 'gene' and 'allele' — a GENE is the trait (e.g. eye colour); an ALLELE is one version of it (e.g. blue or brown). 23 pairs (NOT 23) — be precise.

Question

Adapted from 4BI1/1B May/Jun 2024 Q7(b)6 marks

Compare mitosis and meiosis, referring to chromosome number, number of cell divisions, genetic variation in daughter cells and the role in the organism. (6 marks)

Model answer

Mitosis and meiosis are both forms of nuclear cell division, but they have very different purposes and outcomes.

Comparison table:

Feature	Mitosis	Meiosis
Daughter cells	2	4
Number of divisions	1	2 (Meiosis I + Meiosis II)
Chromosome number	Same as parent (diploid → diploid; 46 → 46)	Halved (diploid → haploid; 46 → 23)
Genetic identity of daughters	IDENTICAL to parent + each other	DIFFERENT from parent + each other
Sources of variation in meiosis	None	Crossing over + independent assortment
Where it happens	All body cells (somatic)	Ovaries and testes only (gamete production)
Purpose	Growth, repair, replacement of cells, asexual reproduction	Production of gametes (sperm and eggs) for sexual reproduction

Mitosis (B1).

ONE division → 2 genetically IDENTICAL daughter cells.
Same chromosome number — DIPLOID stays DIPLOID.
Used for growth (embryo → adult), repair (wound healing), and ASEXUAL reproduction (bacteria, strawberry runners).

Meiosis (B1).

TWO divisions → 4 daughter cells.
Chromosome number HALVED — DIPLOID becomes HAPLOID. (This is essential — when sperm + egg fuse at fertilisation, the DIPLOID number is restored.)
Daughter cells are genetically DIFFERENT because of:
- Crossing over — homologous chromosomes exchange sections during Meiosis I.
- Independent assortment — pairs of chromosomes separate randomly into daughter cells.
Each gamete carries a UNIQUE combination of alleles.
This is the main source of genetic variation in sexual reproduction.

Why the difference matters (B1).

Mitosis preserves the genome (good for replacing cells without losing information).
Meiosis introduces variation (good for adapting the species to a changing environment).
Both are essential — without mitosis you couldn't grow; without meiosis you couldn't have sexual reproduction.

Key marking points: named ploidy (diploid / haploid), variation sources (crossing over, independent assortment), named purpose (growth / repair vs gamete production).

Why this scores

Mark scheme: B1 per contrasted pair, max 6. The most-credited contrasts are: daughter cell number (2 vs 4); chromosome ploidy (diploid vs haploid); genetic identity (identical vs different); purpose (growth/repair vs gametes); number of divisions (1 vs 2); source of variation in meiosis (crossing over + independent assortment). Examiner reports note that 'genetically identical' and 'genetically different' are required keywords.

Question
Adapted from 4BI1/2B January 2024 Q7(b)6 marks
In humans, the ABO blood group is controlled by three alleles: I^A, I^B and i. I^A and I^B are codominant; i is recessive. A man with blood group AB has children with a woman who is heterozygous for blood group A (genotype I^A i). (a) State the possible blood groups of the children and their expected ratio. (b) Explain what is meant by 'codominance'. (6 marks)
Model answer
(a) Genetic cross (4 marks).

Parents:

Father: blood group AB → genotype I^A I^B.

Mother: heterozygous blood group A → genotype I^A i.

Gametes:

Father → I^A or I^B (50% each).

Mother → I^A or i (50% each).

Punnett square:

I^A (mother) i (mother)
I^A (father) I^A I^A I^A i
I^B (father) I^A I^B I^B i

Offspring genotypes and phenotypes:

Genotype Blood group Probability
I^A I^A A 1/4 (25%)
I^A i A 1/4 (25%)
I^A I^B AB 1/4 (25%)
I^B i B 1/4 (25%)

Expected phenotype ratio = 2 A : 1 AB : 1 B = 50% A : 25% AB : 25% B. (Genotype ratio 1 I^A I^A : 1 I^A i : 1 I^A I^B : 1 I^B i.)

(b) Codominance (2 marks).

Codominance is a pattern of inheritance where TWO alleles are BOTH expressed in the heterozygous genotype — neither allele is dominant over the other.

In the ABO system, the genotype I^A I^B produces BOTH A and B antigens on red blood cells → the phenotype is blood group AB.

This is different from standard dominant/recessive inheritance (where only one allele is expressed in the heterozygote).

Other example: sickle-cell anaemia — heterozygotes (Hb^A Hb^S) make both normal and sickle haemoglobin → 'sickle-cell trait' (mild phenotype with some resistance to malaria).
Why this scores
Mark scheme: (a) B1 parental genotypes; M1 Punnett square; A1 offspring genotypes; B1 phenotype ratio stated. (b) B1 BOTH alleles expressed in heterozygote; B1 named example (ABO blood group AB phenotype). Examiner reports note that 'AB' must be specifically described as expressing both antigens — saying 'AB is the mix' is not enough. Use the correct allele symbols (I^A, I^B, i) — not 'A, B, O'.
Question
Adapted from 4BI1/2B May/Jun 2024 Q7(c)5 marks
What is a mutation? Describe its possible effects on an organism and state TWO factors that increase the mutation rate. (5 marks)
Model answer
Definition (B1). A MUTATION is a random, spontaneous CHANGE in the BASE SEQUENCE of DNA. Mutations can be a single base change (point mutation), the loss or addition of bases, or larger chromosomal changes.

How mutations affect the organism:

1. No effect (neutral) (B1). Most mutations occur in non-coding DNA or in regions where the change does not alter the amino acid (degenerate code). These have no observable effect.

2. Harmful effect (B1). A mutation in a coding gene may change an amino acid → produce a non-functional or abnormal protein. Examples:

Sickle-cell anaemia — single base change in the haemoglobin gene → abnormal haemoglobin (HbS) → distorted red blood cells.

Cystic fibrosis — deletion of 3 bases in the CFTR gene → non-functional chloride channel → thick mucus in lungs.

Cancer — mutations in tumour-suppressor genes (e.g. p53) or proto-oncogenes → uncontrolled cell division.

3. Beneficial effect (rare) (B1). Very occasionally, a mutation gives an advantage:

Antibiotic resistance in bacteria — mutation in a target enzyme means antibiotic doesn't bind.

Lactase persistence in adult humans — mutation allows adults to digest milk.

These beneficial mutations are the RAW MATERIAL for natural selection and evolution.

Two factors that increase mutation rate (B1):

Ionising radiation — X-rays, gamma rays, UV light. The high-energy photons damage DNA bases and break DNA strands.

Mutagenic chemicals — e.g. chemicals in tobacco smoke (benzo[a]pyrene), industrial chemicals (asbestos, formaldehyde), some food additives. They modify DNA bases or interfere with replication.

Other factors: heat, certain viruses (insert their DNA), errors during DNA replication.
Why this scores
Mark scheme: B1 definition (change in base sequence); B1 most mutations neutral / harmful / beneficial (any 2 of 3); B1 named example; B1 two factors that increase mutation rate. Examiner reports stress that 'mutation' must be defined as a change in BASE SEQUENCE (NOT 'a change in chromosomes'). Naming a real disease (sickle-cell anaemia / cystic fibrosis) earns the example mark.
Question
Adapted from 4BI1/2B January 2024 Q7(c)7 marks
Red-green colour blindness is a sex-linked recessive disorder caused by an allele on the X chromosome. A colour-blind man marries a woman whose father was colour-blind and whose mother was not. (a) State the genotype of the man. (b) State the genotype of the woman. (c) Calculate the probability that their first child will be a colour-blind girl. Show your reasoning. (7 marks)
Model answer
Symbols. Let X^C = X chromosome with normal allele (dominant). X^c = X chromosome with colour-blindness allele (recessive).

(a) Genotype of the colour-blind man (1 mark). Males are XY. Since the man has colour blindness and the allele is on his single X chromosome, he must carry X^c. His genotype: X^c Y.

(b) Genotype of the woman (2 marks).

Her FATHER was colour-blind → his genotype was X^c Y → he passed his X chromosome (X^c) to all his daughters. So the woman has X^c on one of her X chromosomes.

Her MOTHER was not colour-blind → her mother's X chromosomes were either X^C X^C or X^C X^c. Either way, the maternal X passed to the woman could be X^C or X^c, but the woman is described as not colour-blind herself (implied). For her not to be colour-blind, she must have AT LEAST ONE X^C.

So the woman's genotype is X^C X^c — she is a CARRIER.

(c) Probability of a colour-blind girl (4 marks).

Parental genotypes: Father X^c Y × Mother X^C X^c.

Gametes:

Father: X^c or Y (50% each).

Mother: X^C or X^c (50% each).

Punnett square:

X^C (mother) X^c (mother)
X^c (father) X^C X^c (carrier girl) X^c X^c (colour-blind girl)
Y (father) X^C Y (normal boy) X^c Y (colour-blind boy)

Genotype outcomes (each 25%):

X^C X^c — carrier daughter (normal vision)

X^c X^c — colour-blind daughter

X^C Y — normal son

X^c Y — colour-blind son

Probability of a COLOUR-BLIND GIRL = 1/4 = 25%.

Reasoning summary. For a girl to be colour-blind she must inherit X^c from BOTH parents. The father (X^c Y) passes X^c to all daughters. The mother (X^C X^c) passes X^c to ~50% of all children. So the chance the first child is (a) a girl AND (b) colour-blind = 1/2 × 1/2 = 1/4.
Why this scores
Mark scheme: (a) B1 X^c Y. (b) B1 carrier; B1 X^C X^c. (c) B1 parental genotypes; M1 Punnett square; A1 four genotype outcomes; B1 final answer 1/4 or 25% (must include both 'girl' AND 'colour-blind'). Examiner reports note that candidates often forget that the father passes X^c (not Y) to all daughters → so ALL daughters get an X^c from dad. Use the X^superscript notation throughout.

	I^A (mother)	i (mother)
I^A (father)	I^A I^A	I^A i
I^B (father)	I^A I^B	I^B i

Genotype	Blood group	Probability
I^A I^A	A	1/4 (25%)
I^A i	A	1/4 (25%)
I^A I^B	AB	1/4 (25%)
I^B i	B	1/4 (25%)

	X^C (mother)	X^c (mother)
X^c (father)	X^C X^c (carrier girl)	X^c X^c (colour-blind girl)
Y (father)	X^C Y (normal boy)	X^c Y (colour-blind boy)

Key Definitions and Keywords — Inheritance

Definitions to memorise and the exact keywords mark schemes credit for inheritance answers — sharpened from recent examiner reports for the 2026 Pearson Edexcel IGCSE 4BI1 sitting.

DNA (deoxyribonucleic acid)
Examiner keyword
A double-helix molecule made of two strands of nucleotides. Bases pair complementarily: A-T and C-G. Carries the genetic code in the sequence of bases.
Gene
Examiner keyword
A section of DNA that codes for a specific protein (or polypeptide). The sequence of bases in the gene determines the sequence of amino acids in the protein.
Allele
Examiner keyword
A different version of a gene. For example, the gene for tongue-rolling has two alleles: T (dominant) and t (recessive). Alleles arise by mutation.
Chromosome
Examiner keyword
A long, thread-like structure in the nucleus made of DNA + proteins. Humans have 23 pairs (46 total) in every diploid body cell: 22 pairs of autosomes + 1 pair of sex chromosomes (XX/XY).
Genotype
Examiner keyword
The combination of alleles an organism carries for a particular gene (e.g. Tt, BB, X^h Y). Often written with two letters per gene (one allele from each parent).
Phenotype
Examiner keyword
The observable characteristics of an organism — what its genotype actually looks like (e.g. tongue-roller, blood group A, brown eyes). Influenced by genotype AND environment.
Homozygous
Examiner keyword
Having TWO IDENTICAL alleles for a particular gene (e.g. TT or tt). Often called 'pure-breeding' for that trait.
Heterozygous
Examiner keyword
Having TWO DIFFERENT alleles for a particular gene (e.g. Tt). Often called a 'carrier' when one allele is a recessive disease allele.
Dominant allele
Examiner keyword
An allele that is expressed when present, even if only one copy is inherited (e.g. T in Tt). Written in CAPITALS.
Recessive allele
Examiner keyword
An allele that is only expressed when TWO copies are present (homozygous, e.g. tt). Masked by the dominant allele in heterozygotes. Written in lowercase.
Codominance
Examiner keyword
Pattern of inheritance where BOTH alleles are expressed in the heterozygous genotype — neither allele dominates. Example: ABO blood group — genotype I^A I^B → blood group AB.
Mitosis
Examiner keyword
Nuclear division producing 2 daughter cells genetically identical to the parent cell. Chromosome number stays the same (diploid → diploid). Used for growth, repair and asexual reproduction.
Meiosis
Examiner keyword
Nuclear division producing 4 daughter cells with half the chromosome number (diploid → haploid). Daughter cells are genetically different (crossing over + independent assortment). Used to produce gametes.
Haploid and diploid
Examiner keyword
Haploid (n) = ONE set of chromosomes (gametes, e.g. 23 in human sperm/egg). Diploid (2n) = TWO sets of chromosomes (body cells, e.g. 46 in humans).
Sex-linked inheritance
Examiner keyword
Inheritance of a gene carried on a sex chromosome (usually X). Males (XY) have only one X → they express any X-linked recessive allele they carry. Females (XX) can be CARRIERS (X^H X^h). Examples: haemophilia, red-green colour blindness.
Mutation
Examiner keyword
A random, spontaneous change in the base sequence of DNA. Most are neutral; some are harmful (e.g. cystic fibrosis); rarely beneficial. Causes: ionising radiation, UV, mutagenic chemicals, replication errors.
Natural selection
Examiner keyword
Process by which organisms with advantageous alleles are MORE LIKELY to survive and reproduce → pass alleles to the next generation → frequency of advantageous alleles INCREASES in the population. Steps: variation → selection pressure → survival → reproduction → allele frequency change. (Paper 2 — bold P content.)
Continuous vs discontinuous variation
Examiner keyword
Continuous = range of values, all intermediates possible, normal distribution, polygenic + environmental (e.g. height). Discontinuous = distinct separate categories, no intermediates, monogenic (e.g. ABO blood group, sex).

Common Mistakes and Misconceptions — Inheritance

The traps other students keep falling into on inheritance questions — taken from recent Pearson Edexcel IGCSE 4BI1 examiner reports and mark schemes — and how to avoid them.

✕Using 'gene' and 'allele' interchangeably
4BI1 Examiner Reports 2022-2024
Why it happens
Both relate to inheritance; the distinction is subtle.
How to avoid it
Gene = the characteristic (e.g. gene for tongue-rolling). Allele = one version of the gene (e.g. T or t, the dominant or recessive allele for tongue-rolling). Every gene has at least 2 alleles in a population.
✕Forgetting that meiosis halves the chromosome number
4BI1 Examiner Reports 2024
Why it happens
Confusion between mitosis and meiosis.
How to avoid it
Mitosis: chromosome number STAYS THE SAME (46 → 46 in humans). Meiosis: chromosome number is HALVED (46 → 23). This is essential — gametes MUST be haploid so that when they fuse at fertilisation, the DIPLOID number is restored.
✕Saying organisms 'want to' or 'try to' adapt to their environment (Lamarckian thinking)
4BI1 Examiner Reports 2023-2024
Why it happens
Common misconception that evolution is purposeful.
How to avoid it
Natural selection is NOT purposeful. Variation arises by RANDOM MUTATION before any selection pressure. The environment then SELECTS for organisms that happen to have favourable alleles. Use phrases like 'mutation produced...', 'individuals with X were more likely to survive', 'allele frequency increased' — NOT 'animals developed', 'bacteria wanted to'.
✕Saying sons inherit X from their father
4BI1 Examiner Reports 2024
Why it happens
Forgetting that the father donates X to daughters and Y to sons.
How to avoid it
Father is XY. He passes ONE sex chromosome to each child: X → daughter; Y → son. So sons inherit Y from their father, X from their mother. This is why X-linked recessive disorders (haemophilia, colour blindness) tend to affect males — they have only one X.
✕Drawing a Punnett square correctly but not stating the phenotype ratio
4BI1 Examiner Reports 2022-2024
Why it happens
Stopping at the genotypes.
How to avoid it
ALWAYS state the phenotype ratio in your final answer (e.g. '3 brown : 1 blue', '1 : 1', '50%'). The mark scheme always reserves a mark for the explicit ratio. Both 'ratio' and 'percentage' are accepted, but be clear.
✕Saying mutations are always harmful
4BI1 Examiner Reports 2023
Why it happens
Headlines focus on harmful mutations (cancer, genetic disease).
How to avoid it
MOST mutations are neutral (no effect). SOME are harmful (e.g. sickle-cell anaemia). RARELY a mutation is beneficial (e.g. antibiotic resistance in bacteria, lactase persistence). Beneficial mutations are the RAW MATERIAL of evolution — without them, no natural selection.
✕Saying eye colour is discontinuous variation
4BI1 Examiner Reports 2024
Why it happens
Simplification in textbooks.
How to avoid it
Eye colour is actually CONTINUOUS (many shades of brown, hazel, green, blue, grey) — it is polygenic. The classic exam-safe example for DISCONTINUOUS variation is ABO blood group (only A, B, AB, O). For CONTINUOUS: height, body mass, foot length.
✕Saying 'the individual evolves' or 'the bacterium became resistant'
4BI1 Examiner Reports 2024
Why it happens
Misunderstanding of how evolution works.
How to avoid it
Individuals do NOT evolve. POPULATIONS evolve. The individual either has the advantageous allele (and survives) or doesn't (and may die). Over generations, the frequency of advantageous alleles increases in the POPULATION → this is evolution.

Practice questions

Exam-style questions with step-by-step worked solutions. Try one before checking the method.

Past paper style quiz

Get a report showing which sub-topics you've nailed and which ones still need work.

Video lesson

Short walkthrough of the concepts students most often get stuck on.

Inheritance — frequently asked questions

The things students keep getting wrong in this sub-topic, answered.

Inheritance

Short Study Notes in the form of Slides

Detailed Study Notes

What you’ll learn

How it’s examined

1Distinguish between mitosis and meiosis (5 marks, Paper 1)

2Punnett square for a monohybrid cross (5 marks, Paper 1)

3Sex linkage — haemophilia inheritance (5 marks, Paper 2)

4Natural selection — antibiotic resistance in bacteria (6 marks, Paper 2)

5Continuous vs discontinuous variation (4 marks, Paper 1)

DNA (deoxyribonucleic acid)

Gene

Allele

Chromosome

Genotype

Phenotype

Homozygous

Heterozygous

Dominant allele

Recessive allele

Codominance

Mitosis

Meiosis

Haploid and diploid

Sex-linked inheritance

Mutation

Natural selection

Continuous vs discontinuous variation

✕Using 'gene' and 'allele' interchangeably

✕Forgetting that meiosis halves the chromosome number

✕Saying organisms 'want to' or 'try to' adapt to their environment (Lamarckian thinking)

✕Saying sons inherit X from their father

✕Drawing a Punnett square correctly but not stating the phenotype ratio

✕Saying mutations are always harmful

✕Saying eye colour is discontinuous variation

✕Saying 'the individual evolves' or 'the bacterium became resistant'

Practice questions

Past paper style quiz

Assess your understanding

Video lesson

Inheritance — frequently asked questions