Gene expression

Practice

Recall it first, then use it — testing yourself builds the memory, where rereading the notes above only feels easier.

Recall and application shuffled together — you have to work out what each item wants before you can answer it, which is the part the exam actually tests. Both kinds feed the same spacing schedule, so anything you miss comes back sooner.

Say the answer out loud before flipping — that attempt is where the learning happens, even when you get it wrong.

Exam-style only. Instant feedback, shuffled each attempt, best score saved on this device.

What actually comes up

Three "discuss" questions every year, each opening with a diagram or table to complete (worth the Achieved marks) before a full extended-writing discussion (worth Merit and Excellence). A mutation-severity question, a protein-synthesis "why two steps, not one" question, and a genotype-environment-phenotype metabolic-pathway question recur in some form every year, each built around a different real biological context.

Across 4 years

The pattern — what to prepare

The 2025 paper ↗ Marking schedule ↗

Question One — Mutation effects on protein (cystic fibrosis)

The CFTR gene's normal DNA/mRNA/amino-acid sequence is given, alongside two mutated versions, using the provided codon table.

• Normal: TTA TGC AAT CCG → AAU ACG UUA GGC → Asn Thr Leu Gly
• Mutated 1: TTA TGC GAT CCG
• Mutated 2: TTA TGC AAG CCG

• a Complete the mRNA and amino acid sequences for both mutated DNA sequences using the codon table. Achieved
• b (achieved) Identifies both as substitution point mutations with no frameshift, and describes substitution as less severe than a frameshift. Achieved
• b (merit) Explains mutation 1 as a silent substitution (no amino acid change, due to degeneracy) and mutation 2 as a substitution changing one amino acid (Leu→Phe), causing only a small functional change. Merit
• b (excellence) Provides detailed discussion of mutation 1's effect on the CFTR protein (no symptoms) versus mutation 2's effect (symptoms occur), and why a substitution is less severe than an insertion/deletion frameshift. Excellence

Question Two — Protein synthesis

A transcription diagram to complete, then a discussion of why DNA cannot be directly translated.

• a Complete a transcription diagram: template strand, complementary mRNA, sugars, phosphates, and the 5'/3' ends. Achieved
• b (achieved) Describes a codon, anticodon, tRNA and mRNA structure, transcription's start/end point, translation's start/end point, and ONE valid reason DNA is not directly translated. Achieved
• b (merit) Explains the process of transcription (start/stop points, base pairing, elongation, occurring in the nucleus) and translation (occurring at ribosomes, start/stop codons, polypeptide formation), and how codons/anticodons match. Merit
• b (excellence) Provides detailed discussion linking transcription and translation into one coherent account, with TWO well-justified reasons why DNA cannot be directly translated into a polypeptide. Excellence

Question Three — Chlorophyll and chlorosis

A two-gene, two-enzyme metabolic pathway converts glutamate to chlorophyll, needing magnesium at the second step.

• Gene 1 → Enzyme 1: glutamate → intermediate substrate
• Gene 2 → Enzyme 2 (+ magnesium): intermediate → chlorophyll

• achieved Describes a metabolic pathway and an enzyme, that gene 1 codes for enzyme 1 and gene 2 for enzyme 2, that both must be functional for chlorophyll, and that enough magnesium makes chlorophyll. Achieved
• merit Explains the relationship between the two genes, two enzymes and three molecules in the pathway, how low magnesium prevents enzyme 2 working, and how a mutation in either gene stops chlorophyll production causing chlorosis. Merit
• excellence Discusses how normal genotype interacts with magnesium availability to determine leaf colour, and that a mutation in either gene produces chlorosis regardless of how much magnesium is available. Excellence

The 2022 paper ↗ Marking schedule ↗

Question One — Protein synthesis

Translation is a key step in protein synthesis.

• achieved Describes translation, codon, anticodon, mRNA, tRNA, amino acids, a polypeptide chain, protein synthesis, and why DNA is not directly translated. Achieved
• merit Explains translation including a start or stop codon, mRNA's function carrying the message to the ribosome, tRNA's function linking codon to amino acid, and why DNA is not directly translated. Merit
• excellence Discusses the relationship between codons, anticodons, tRNA, mRNA and amino acids, AND justifies TWO reasons why DNA is not directly translated into a polypeptide chain. Excellence

Question Two — The genetic code (albinism)

A mutation in the gene coding for the enzyme tyrosinase causes albinism, decreasing melanin production.

• a Describe what a mutation is. Achieved
• b (achieved) Describes insertion, deletion and substitution, describes degeneracy of the code, and identifies which point mutation is unlikely to change the protein and which is most likely to. Achieved
• b (merit) Explains why substitution has the least effect (may code for the same amino acid, no frameshift, length/start/stop codons unchanged) and why insertion/deletion have a major effect (frameshift changes the amino acid sequence, shape, and function). Merit
• b (excellence) Comprehensively discusses how degeneracy buffers a substitution's effect, and how an insertion or deletion shifts the reading frame from that point onward, changing the protein's folding, structure and function. Excellence

Question Three — Gene expression and environment (Himalayan rabbits)

Himalayan rabbits show temperature-sensitive albinism: the melanin-producing enzyme is active below 25°C and inactive above 30°C; average body temperature is 37°C.

• achieved Describes a precursor/substrate, intermediate/final product, enzyme, metabolic pathway, that genes code for enzymes, genotype+environment=phenotype, and that the enzyme works at low temperatures to produce melanin. Achieved
• merit Explains the relationship between genes, enzymes and products in this pathway, and how genotype interacts with temperature: warm core body deactivates tyrosinase (white), cooler extremities keep it functional (black). Merit
• excellence Explains the metabolic pathway AND comprehensively discusses that the SAME genotype (same tyrosinase enzyme) is present throughout, with environmental temperature alone determining fur colour across the rabbit's lifespan. Excellence

The 2024 paper ↗ Marking schedule ↗

Question One — Protein synthesis

Three differences between DNA and mRNA; tRNA is more stable than mRNA, which breaks down within hours.

• a Complete a table describing three ways mRNA and DNA differ from each other. Achieved
• b (achieved) Describes protein synthesis, mRNA's function carrying the message to the ribosome, tRNA's function and cloverleaf structure, and transcription as the process that makes mRNA. Achieved
• b (merit) Explains mRNA carrying a gene section from nucleus to ribosome, tRNA carrying a specific amino acid, codon/anticodon complementarity, and why mRNA is unstable (single-stranded, unprotected). Merit
• b (excellence) Discusses how mRNA and tRNA together transfer the genetic code to the ribosome via complementary base pairing, and the significance of their differing structure and stability for protein synthesis. Excellence

Question Two — Mutations (β-globin/haemoglobin)

The normal and mutated DNA template strand for part of the β-globin gene are given, with a triplet-to-amino-acid reference table.

• Normal: TGA GGA CTC CTC
• Mutated: TGA GGA CAC CTC

• a Complete tables of mRNA, tRNA, and amino acid sequences for the normal and mutated β-globin DNA sequences. Achieved
• b (achieved) Describes/identifies two causes of mutations, that this is a substitution with no frameshift, a mutagen, and a negative consequence (haemoglobin not working correctly). Achieved
• b (merit) Explains a mutagen with two examples, that the substitution changes one amino acid causing a small functional change, and that no frameshift means no large downstream change. Merit
• b (excellence) Discusses the mutation's effect on the beta-globin polypeptide's shape and function, and compares this substitution (missense) against an insertion/deletion frameshift in severity. Excellence

Question Three — Haem synthesis and anaemia

A metabolic pathway synthesises haem for haemoglobin; low iron and high lead can both limit haem production.

• achieved Describes a metabolic pathway, an enzyme, that genes code for specific enzymes, that a mutation to either gene can cause anaemia, and that genotype+environment=phenotype. Achieved
• merit Explains the relationship between the two genes, two enzymes and three molecules in the pathway, how a mutation stops haem being made, and how low iron or high lead each prevent enzyme 2 from working. Merit
• excellence Discusses this specific metabolic pathway comprehensively, including how anaemia can arise from a mutation in gene 1, gene 2, or environmental factors (low iron, high lead) without any mutation at all. Excellence

The 2023 paper ↗ Marking schedule ↗

Question One — Mutations

A normal gene sequence and two point mutations are given (affected bases marked), using the provided codon table.

• Normal: TAA TAG ATA CCA CAA
• Mutation 1: TAA TAG ATG CCA CAA
• Mutation 2: TAA TAG ATT CCA CAA

• a Complete the mRNA strand and amino acid sequence for the normal gene and both point mutations. Achieved
• b (achieved) Describes mutation 1 as silent/same-sense and mutation 2 as coding for STOP (nonsense), identifies both as substitutions, and identifies which will and won't change the final protein. Achieved
• b (merit) Explains that mutation 1 does not change the amino acid sequence (protein folds correctly) while mutation 2 changes it to a stop codon (shorter, incorrectly-folding protein), linking to degeneracy of the code. Merit
• b (excellence) Comprehensively discusses why mutation 1 leaves the start/stop codons, length and folding unaffected, contrasted with mutation 2's effect on protein length, folding and function. Excellence

Question Two — Genotype, environment, and mutagens

A gene → enzyme → melanin pathway is affected by UV light, which is non-mutagenic at low levels (triggering melanin production) and mutagenic at high levels; people with albinism cannot produce melanin.

• Gene 1 → Enzyme 1: phenylalanine → tyrosine
• Gene 2 → Enzyme 2 (+ UV as a non-mutagenic trigger): tyrosine → melanin

• achieved Describes an environmental factor changing phenotype not genotype, a mutagen, a metabolic pathway, that genes code for the enzymes, and states that albinism means no melanin is made. Achieved
• merit Explains the full metabolic pathway, how UV increases enzyme 2 production (more melanin, non-mutagenic effect), and how albinism arises when gene 2/enzyme 2 is dysfunctional so no melanin is made. Merit
• excellence Comprehensively discusses how low-level UV changes phenotype without changing genotype, versus how high-level UV can itself mutate gene 2, explaining the greater skin cancer risk without melanin's protection. Excellence

Question Three — Protein synthesis

A DNA structure diagram to complete, then a discussion of base-pairing accuracy in protein synthesis.

• a Complete a DNA diagram: template strand, complementary antiparallel strand, sugars, and phosphates. Achieved
• b Name the two stages of protein synthesis and the order in which they occur. Merit
• c (achieved) Describes a triplet, a codon, an anticodon, and the base-pairing rule, and states that inaccurate transcription/translation leads to an incorrect amino acid sequence/protein shape. Achieved
• c (merit) Explains why C binds G and A binds T/U (hydrogen bonds and purine/pyrimidine size), that triplets/codons determine amino acids, and why triplets must become codons to leave the nucleus for translation. Merit
• c (excellence) Discusses, with full understanding, why base-pairing accuracy at BOTH transcription and translation is required for the final protein to fold correctly and function. Excellence

Grades above are read from each year's own Achievement/Merit/Excellence evidence statement, condensed to the actual task — the schedules also grade holistically per question on a 0–8 scale, not a fixed mark per bullet.

Past exams & resources

⏱ Timed opens the paper and starts a countdown matching the exam length. Official NZQA PDFs. If a link 404s, that year’s paper may sit under a slightly different code: browse the NZQA subject page.