Q: What does CORE IDEAS, Topic 2 - Genetics and Inheritance cover?
A: Master DNA architecture, chromatin control, genetic exchange in microbes, meiotic variation, and multi-gene inheritance so you can tackle 2026 H2 Biology genetics essays and data tasks with confidence.
Why genetics drives Paper 2, Paper 3, and SPA
Breadth of questioning: Expect DNA replication or gene regulation in structured questions, mutation and cancer essays in Paper 3, and chi-squared verification of ratios in Paper 4 data analysis.
Links across syllabus: Genetics underpins evolution, biotechnology, and even physiology (e.g. insulin regulation). You need both molecular detail and probability fluency.
SEAB emphasis: The 2026 syllabus expands microbial genetics, epigenetics, and ethical dimensions of screening-frequent sources of novel scenario questions.
Syllabus snapshot
DNA structure, chromatin levels (nucleosome to metaphase chromosome)
Central dogma: replication, transcription, translation, and regulation
Viral and bacterial genetics: lytic/lysogenic cycles, horizontal gene transfer
Genome organisation, mutations, and cancer genomics
Cell cycle control, mitosis, and meiosis
Mendelian, non-Mendelian, and multi-factorial inheritance
), complementary base pairing (A–T via two hydrogen bonds, G–C via three). Emphasise phosphodiester backbone directionality for referencing replication enzymes.
Chromatin packaging: Progress from nucleosome (histone octamer + ≈147bp DNA) to 30 nm fibre, loops, and metaphase chromosome. Discuss histone tail acetylation (loosens chromatin, enabling transcription) vs methylation (context-dependent). Link to epigenetics questions about environmental effects on gene expression.
Genome organisation: Contrast exons, introns, regulatory sequences (promoters, enhancers), repetitive DNA, and transposable elements. Explain why prokaryotes lack introns and typically have operons.
Practice sketch
Draw and annotate a nucleosome, labelling DNA directionality and indicating how histone acetylation alters transcriptional accessibility.
Concept 2: Flow of genetic information
Replication: Semi-conservative replication with origins, replication forks, leading and lagging strands. Highlight enzymes: helicase, DNA polymerase III/I, primase, ligase, topoisomerase. Stress proofreading and mismatch repair; mention how defects (MLH1 mutations) increase cancer risk.
Transcription and RNA processing: RNA polymerase binding to promoter (TATA box in eukaryotes), formation of pre-mRNA, capping, polyadenylation, splicing (role of spliceosome). Introduce alternative splicing for proteome diversity.
Translation: Initiation (small ribosomal subunit binds the mRNA cap, initiator tRNA carrying Met enters the P site), elongation (codon–anticodon pairing, peptidyl transferase), termination (release factors). Distinguish 80S eukaryotic vs 70S prokaryotic ribosomes.
Gene regulation: Describe transcription factors, enhancers, silencers, DNA methylation. Compare prokaryotic operon control-lac operon (inducible) vs trp operon (repressible).
Application prompt
Explain how lac operon control illustrates negative and positive regulation. Extend by predicting β-galactosidase expression when glucose is absent but lactose is present.
Concept 3: Viral and bacterial genetics
Viruses: Lytic vs lysogenic cycles; describe integration as a prophage and triggers for induction. RNA viruses rely on RNA-dependent RNA polymerases with high mutation rates (ties to antigenic drift).
Bacteria: Conjugation (F plasmid pilus), transformation (uptake of naked DNA), transduction (phage-mediated). Each mechanism introduces genetic variation without sexual reproduction-ideal comparison to meiosis essays.
CRISPR-Cas systems: Adaptive immunity in bacteria; potential question on biotechnology ethics.
Worked scenario
Given colony growth on antibiotic media, determine whether resistance arose via spontaneous mutation or horizontal transfer. Require referencing fluctuation tests and plasmid profiling.
Concept 4: Mutation, cancer, and genomics
Gene mutations: Point mutations (missense, nonsense, silent), insertion/deletion (frameshift). Use sickle cell anaemia (Glu6Val) as example of structure-function consequence. Highlight trinucleotide repeat expansions (Huntington’s disease) for Paper 3 essays.
Chromosomal aberrations: Numerical (aneuploidy-trisomy 21 via nondisjunction) vs structural (translocation, inversion, duplication, deletion). Emphasise meiotic origin.
Cancer genetics: Distinguish proto-oncogene activation (ras gain-of-function) vs tumour suppressor loss (p53). Detail multistep model: accumulation of mutations, angiogenesis, metastasis. Introduce hallmarks (evading apoptosis, replicative immortality).
Meiosis: Reduction division; homologous chromosome pairing, crossing-over (chiasmata), independent assortment. Distinguish Meiosis I (reductional) vs Meiosis II (equational). Stress sources of variation: crossing-over, random assortment, random fertilisation.
Practical angle
Design a Paper 4 investigation to observe meiosis in onion anthers: staining (acetic orcein), squash preparation, stage identification, and data logging for PDO and ACE.
Monohybrid and dihybrid crosses: Use Punnett squares and probability trees, incorporating codominance (ABO blood groups) and incomplete dominance (snapdragon colour).
Multiple alleles, epistasis, linkage: Work through dihybrid ratio deviations. Show how test crosses reveal linkage; map units approximate recombination frequency.
Sex linkage: X-linked recessive examples (haemophilia). Explain why males exhibit more frequently (hemizygous).
Environmental influence: Honeybee caste differentiation via diet; human height (polygenic, environmental).
Chi-squared practice
Given observed pea plant phenotypes (315 round yellow, 108 round green, 101 wrinkled yellow, 32 wrinkled green), calculate expected counts for a 9:3:3:1 ratio, compute χ2, compare with critical value at ν=3, and interpret whether to reject Mendelian segregation.
Concept 7: Population genetics tools
Use the Hardy–Weinberg equation p2+2pq+q2=1 with p+q=1 to model allele frequencies. Discuss assumptions (large population, random mating, no mutation/migration/selection). Apply to carrier screening scenarios:
If q=0.02, calculate expected carrier frequency 2pq=2(0.98)(0.02)=0.0392.
Evaluate how selection or migration disrupts equilibrium.
Introduce R0 (basic reproductive number) for pathogen spread as a bridge to infectious disease extension content.
Exam technique checkpoints
Paper 2: Practise interpreting pedigree charts and micrographs of cell division. Always state genotype with alleles (e.g. Rr) before phenotype.
Paper 3: Prepare essay outlines on “From mutation to cancer” and “Regulation of gene expression in eukaryotes vs prokaryotes.”
Paper 4: Run simulated chi-squared tests using yeast genetics or Drosophila crosses; justify sampling strategy, degrees of freedom, and use of null hypotheses.
