BIOSCI 107 Biology for Biomedical Science: Cellular Processes and Development
BIOSCI 107 Overview
- University of Auckland
- S1 2027
- 11 chapters
- Biology
BIOSCI 107 Biology for Biomedical Science: Cellular Processes and Development is the University of Auckland's Stage I cell-and-development biology course — 15 points in the Faculty of Science (School of Biological Sciences), and one of the core first-year courses biomedical-science students take before applying for clinical-programme selection.
- Assessed by Final Exam 40% · Mid-Semester Test 30% · Practical (labs + pre-labs) 20% · Online Feedback Quizzes 10%
- Key terms Theory hurdle, Teleform (paper MCQ), Nernst equation, Cross-bridge cycle
- How to prepare Treat the course as two halves with two exams.
- Most asked Where can I find past exam papers / practice for BIOSCI 107?
What you get in the full BIOSCI 107 Exam Bible
- 11 chapters, 115 pages — every examinable topic, week by week
- 29 original practice questions in the Final Exam format
- 11 worked examples, solved the way BIOSCI 107 marks
- 35 computed figures, redrawn from the course’s own numbers
- Exam-morning plan for the Final Exam (40%) — what to revise last, where marks are lost
Free on this page: assessment table, chapter map, one worked example, key terms, FAQ. The rest is in the full exam bible.
How BIOSCI 107 is assessed
| Component | Weight | Format |
|---|---|---|
| Final Exam | 40% | UoA S1 exam period; in-person, on paper (Teleform MCQ), 2 h, ~90 marks, sections A–D, covers Topics 4–7 |
| Mid-Semester Test | 30% | In-semester evening test; on paper (Teleform MCQ), 90 min, 70 questions, covers Topics 1–3 |
| Practical (labs + pre-labs) | 20% | Laboratory sessions across the course; lab coat + safety glasses required |
| Online Feedback Quizzes | 10% | Weekly; 12 activities (best 10 count) — topic quizzes, PeerWise, mock test/exam |
What other students are asking about BIOSCI 107
- Where can I find lecture notes or study guides for BIOSCI 107 at Auckland?
- The BIOSCI 107 study guide in AskSia Library covers Biology for Biomedical Science: Cellular Processes and Development in 11 chapters, with the assessment table, a chapter-by-chapter topic map, key terms and a worked example, free to read on this page.
- Is there a final exam in BIOSCI 107, and how much is it worth?
- Yes. In the offering this AskSia Library guide is built from, Final Exam carries 40% of the BIOSCI 107 mark; the full split is Final Exam 40%, Mid-Semester Test 30%, Practical (labs + pre-labs) 20%, Online Feedback Quizzes 10%.
- What does BIOSCI 107 cover on cell structure & cellular respiration?
- In AskSia Library's BIOSCI 107 guide, the Cell Structure & Cellular Respiration chapter explains organelles & cytoskeleton · glycolysis → citric-acid cycle → oxidative phosphorylation (~30–32 ATP) · PFK control · insulin/glucagon (Topic 2 · Test).
- What does BIOSCI 107 cover on cell communication & signalling?
- In AskSia Library's BIOSCI 107 guide, the Cell Communication & Signalling chapter explains gPCRs · ligand-gated ion channels · phosphorylation cascades · the cAMP and Ca²⁺/IP₃ second messengers (Topic 2 · Test).
- What does BIOSCI 107 cover on gene expression, cell division & cancer?
- In AskSia Library's BIOSCI 107 guide, the Gene Expression, Cell Division & Cancer chapter explains transcription → RNA processing → translation · protein sorting · mitosis vs meiosis & checkpoints (MPF) · proto-oncogenes & tumour-suppressors (Topic 2 · Test).
What BIOSCI 107 covers
The whole course → one exam-ready map. Topics 1–3 (Cells & Tissues, Cell Structure & Function, and the Special Topics on development and proteins) are the entire territory of the 30% mid-semester test; Topics 4–7 (membrane transport, blood & immunity, neurons and muscle) are examined in the 40% final exam — both on paper as Teleform multiple-choice.
Labs (20%) and online feedback quizzes (10%) round out the mark, and a theory + practical hurdle sits over the lot. Each chapter links to its free guide.
Cells, Tissues & Body Organisation
The 11 body systems · 4 tissue types · epithelia (cell junctions, basement membrane), connective tissue (the ECM), muscle & nerve tissue (Topic 1 · Test)Topic 1 of University of Auckland BIOSCI 107 lays the structural groundwork: the six levels of organisation, the eleven body systems, and the four primary tissue types — epithelial, connective, muscle and nerve.
- Six levels of organisation (chemical → cellular → tissue → organ → system → organismal) and the 11 body systems
- The four primary tissue types: epithelial (cover/line/glands), connective (cells in matrix), muscle (contractile), nervous (conducting)
- Epithelial classification: arrangement (simple/stratified/pseudostratified) × shape (squamous/cuboidal/columnar/transitional); the outer layer names a stratified epithelium
- Cell junctions and their linker proteins: tight (occludin/claudin), adherens (cadherin→actin), desmosome (cadherin→keratin), hemidesmosome (integrin→laminin), gap (connexins)
- The basement membrane = basal lamina (from epithelium) + reticular lamina (from fibroblasts); epithelia are avascular
- Connective tissue = ECM (ground substance + fibres) + cells; three fibre types (collagen, reticular, elastic)
Cell Structure & Cellular Respiration
Organelles & cytoskeleton · glycolysis → citric-acid cycle → oxidative phosphorylation (~30–32 ATP) · PFK control · insulin/glucagon (Topic 2 · Test)Topic 2 opens with the eukaryotic cell — the plasma membrane, the organelles and the three cytoskeletal filaments — then follows a glucose molecule through cellular respiration: glycolysis, pyruvate oxidation, the citric-acid cycle and oxidative phosphorylation, for a maximum of about 30–32 ATP.
- The plasma membrane: phospholipid bilayer (polar heads out, tails in), fluid mosaic, integral vs peripheral proteins
- Organelles: nucleus/nucleolus, ribosomes (free vs RER-bound), rough & smooth ER, Golgi, mitochondria (not part of the endomembrane system)
- The cytoskeleton: microfilaments (actin), intermediate filaments (keratin), microtubules (tubulin — chromosome movement, cilia/flagella)
- Cellular respiration overview: C₆H₁₂O₆ + 6 O₂ → 6 CO₂ + 6 H₂O + energy
- The four stages, their locations and ATP yields: glycolysis (cytosol, +2), pyruvate oxidation (matrix, 0), citric-acid cycle (matrix, +2), oxidative phosphorylation (inner membrane, ~26–28)
- Substrate-level vs oxidative phosphorylation; O₂ as the final electron acceptor; chemiosmosis and ATP synthase
Cell Communication & Signalling
GPCRs · ligand-gated ion channels · phosphorylation cascades · the cAMP and Ca²⁺/IP₃ second messengers (Topic 2 · Test)Topic 2 continues with how cells talk to each other: the three universal steps (reception → transduction → response), the main receptor classes (G-protein-coupled receptors and ligand-gated ion channels), phosphorylation cascades, and the second messengers cAMP and Ca²⁺/IP₃.
- Signalling range: paracrine (local), synaptic (neurotransmitters), autocrine (on self), endocrine (hormones via blood to distant targets)
- The three steps: reception (ligand binds, shape change) → transduction (cascade + second messengers) → response
- Receptor location by ligand solubility: water-soluble → membrane receptors; lipid-soluble (steroids) → cytoplasmic/nuclear receptors
- G-protein-coupled receptors (7-transmembrane) and the G-protein switch: GDP = off, GTP = on; GTPase resets
- Ligand-gated (ionotropic) ion channels — fast, used heavily by the nervous system
- Phosphorylation cascades: kinases add phosphate (activate), phosphatases remove it (reset); amplification and multiple control points
Gene Expression, Cell Division & Cancer
Transcription → RNA processing → translation · protein sorting · mitosis vs meiosis & checkpoints (MPF) · proto-oncogenes & tumour-suppressors (Topic 2 · Test)Topic 2 finishes with the flow of genetic information and how cells divide.
- Central dogma DNA → RNA → protein; transcription (initiation/elongation/termination), RNA polymerase II at the promoter (TATA box), RNA uses uracil
- RNA processing in order: 5′ cap, 3′ poly-A tail, splicing (spliceosome removes introns, joins exons); alternative splicing
- Translation: mRNA read 5′→3′, protein made N→C; ribosome A/P/E sites; peptide bonds catalysed by rRNA (ribozyme); stop codons UAA/UAG/UGA
- Protein sorting: signal peptide + SRP direct the ribosome to the rough ER; post-translational modifications
- The cell cycle: interphase (G1, S, G2) + M phase; G0 exit; mitosis (2n→2n identical) vs meiosis (2n→1n, variable)
- Meiosis I separates homologous chromosomes (crossing-over, independent assortment); meiosis II separates sister chromatids
Early Development & Protein Structure
Fertilisation → gastrulation · the 3 germ layers · the stem-cell hierarchy & CRISPR · protein 1°–4° structure & the force hierarchy (Topic 3 · Test)Topic 3, the Special Topics, pairs early human development with protein structure.
- Week 1: fertilisation (n + n → 2n) → cleavage (rapid mitosis, cells shrink, no growth) → morula → blastocyst (inner cell mass + trophoblast + cavity) → implantation
- Gastrulation via the primitive streak generates the three germ layers, all derived from the epiblast
- Germ-layer derivatives: ectoderm (epidermis + all nervous tissue), mesoderm (all muscle, cardiovascular, skeleton, kidney), endoderm (gut/respiratory epithelium, liver, pancreas)
- The stem-cell hierarchy by potency: totipotent → pluripotent (inner cell mass/ESCs/iPSCs) → multipotent → unipotent
- CRISPR/Cas9: targeted DNA cuts using the cell's own repair machinery; versatile across cell types
- The peptide bond: a covalent bond between one amino acid's carboxyl and another's amino group, formed by dehydration (condensation)
Membrane Transport & Epithelial Function
Passive vs active transport · the Na⁺/K⁺-ATPase · osmosis & aquaporins · SGLT/GLUT & the renal threshold · NKCC/CFTR, cholera & cystic fibrosis (Topic 4 · Exam §B)Topic 4 (exam Section B) is the first of the exam-only topics: how molecules cross membranes.
- Transport axes: non-mediated vs mediated (protein), and passive (down gradient, no energy) vs active (against gradient, energy)
- Simple diffusion of nonpolar molecules (O₂, CO₂, steroids, fat-soluble vitamins) straight through the bilayer
- Ion channels (fast, selective, gated) vs carriers (slower, enzyme-like: specificity, competition, saturation/transport maximum)
- Primary active transport: the Na⁺/K⁺-ATPase (3 Na⁺ out : 2 K⁺ in, electrogenic, ~30% of cell energy)
- Secondary active transport: symporters (Na⁺-glucose) and antiporters (Na⁺/Ca²⁺) powered by the Na⁺ gradient
- Osmosis and water permeability Pw = Pd (bilayer) + Pf (aquaporins)
Blood & the Immune System
Blood & the coagulation cascade · complement (C3b opsonisation, the MAC) · antibodies & V(D)J recombination · MHC I→CD8 / MHC II→CD4 (Topic 5 · Exam §A)Topic 5 (exam Section A) covers blood and defence: blood composition, haemoglobin and the coagulation cascade; the innate system and complement (C3b opsonisation, the membrane attack complex); antibodies and V(D)J recombination (the five Ig classes, affinity vs avidity, RAG1/2, clonal selection); and cellular immunity and MHC restriction — MHC class I to CD8 cytotoxic T cells, MHC class II to CD4 helper T cells — plus allergy and hypersensitivity.
- Blood composition: plasma (55%, has fibrinogen) vs serum; formed elements (RBC 45%, buffy coat of WBC + platelets); centrifuged order bottom→top
- Haemoglobin loads/unloads O₂ by partial pressure; CO/cyanide displace O₂ (CO → cherry-red blood)
- Haematopoiesis from the HSC (CD34⁺ marker) → myeloid and lymphoid lineages
- Coagulation cascade: intrinsic + extrinsic pathways converge on Factor X → thrombin → fibrinogen to fibrin (Ca²⁺ essential)
- Complement: three pathways converge on C3; C3b opsonises (binds covalently); MAC (C5–C9) lyses; anaphylatoxins C3a/C5a
- Innate immunity: barriers, phagocytes (neutrophils most abundant), NK cells, pattern-recognition receptors
Neurons: Membrane Potential & Action Potentials
The Nernst & Goldman equations · the Na⁺/K⁺ pump & leak channels · voltage-gated Na⁺/K⁺ channels · refractory periods · saltatory conduction (Topic 6 · Exam §C)Topic 6 (exam Section C) is the course's one quantitative topic.
- Resting membrane potential (−50 to −70 mV); only neurons and muscle are 'excitable'
- The ionic set-up: [K⁺]ᵢ high / [K⁺]ₒ low and [Na⁺]ᵢ low / [Na⁺]ₒ high, maintained by the Na⁺/K⁺ pump (3 out : 2 in); many leak K⁺ channels → resting P_K/P_Na ≈ 40:1
- Nernst equation E_ion = 61.5 mV × log₁₀([ion]ₒ/[ion]ᵢ): E_K ≈ −80 mV, E_Na ≈ +62 mV (permeable to one ion only)
- Goldman equation: Vm = 61.5 × log₁₀[(P_K[K]ₒ + P_Na[Na]ₒ)/(P_K[K]ᵢ + P_Na[Na]ᵢ)]; RMP sits near E_K because P_K ≫ P_Na
- Rule: raising permeability to an ion pulls Vm toward that ion's equilibrium potential
- Action potential stages: depolarisation (VG Na⁺ activate) → repolarisation (Na⁺ inactivate, VG K⁺ open) → after-hyperpolarisation
Synaptic Transmission
The neuromuscular junction · EPSPs & IPSPs · neurotransmitter classes & inactivation · spatial & temporal summation (Topic 6 · Exam §C)Topic 6 continues into how neurons pass a signal on: the neuromuscular junction as the excitatory model, excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs), the neurotransmitter classes and how they are inactivated, and the spatial and temporal summation that lets tiny inputs add up to threshold.
- The neuromuscular junction: presynaptic AP → voltage-gated Ca²⁺ influx → ACh release → ligand-gated cation channels → end-plate potential (always suprathreshold)
- Steps of chemical transmission: AP arrives → Ca²⁺ enters → vesicle exocytosis → transmitter binds receptor → postsynaptic potential
- EPSP (depolarising; glutamate/ACh; Na⁺/K⁺ channels) vs IPSP (hyperpolarising; GABA/glycine; K⁺ or Cl⁻)
- Neurotransmitter classes: small-molecule/classical (fast, direct — glutamate, GABA, glycine, ACh, amines) vs neuropeptides (slow, modulatory)
- Inactivation: diffusion, enzymatic degradation (acetylcholinesterase on ACh), and re-uptake by transporters
- Integration at the axon initial segment: each synapse gives a tiny (~0.1 mV) potential
Skeletal Muscle: Contraction & Mechanics
The sliding-filament model & cross-bridge cycle · the Ca²⁺/troponin/tropomyosin trigger · excitation–contraction coupling · length–tension · motor units (Topic 7 · Exam §D)Topic 7 (exam Section D) opens with skeletal muscle: the sarcomere and the sliding-filament model, the four-step cross-bridge cycle with its Ca²⁺/troponin/tropomyosin trigger, excitation–contraction coupling from the neuromuscular junction to SR Ca²⁺ release, the length–tension relationship, muscle metabolism and motor units.
- Sarcomere anatomy: thick (myosin) A band, thin (actin) I band, H zone, Z-disc, M line, titin; T-tubules and the sarcoplasmic reticulum (SR) as Ca²⁺ store
- Thin-filament regulation: troponin (binds Ca²⁺) + tropomyosin (blocks myosin-binding sites on actin)
- Sliding-filament theory: Z-lines pulled toward the M-line; I band and H zone narrow; the A band stays constant
- The four-step cross-bridge cycle: cross-bridge formation → power stroke → detachment (needs new ATP) → re-energisation (ATP hydrolysed)
- Role of Ca²⁺: binds troponin → tropomyosin shifts → exposes actin's myosin-binding sites; no ATP → rigor
- Excitation–contraction coupling: motor AP → ACh → end-plate potential → muscle AP → T-tubule → SR Ca²⁺ release → contraction; Ca²⁺-ATPase pumps Ca²⁺ back to relax
Cardiac & Smooth Muscle
The cardiac plateau AP & CICR · the SA node & Starling's law · smooth-muscle calmodulin–MLCK (no troponin) — contrasted with skeletal muscle (Topic 7 · Exam §D)Topic 7 (exam Section D) closes by contrasting the other two muscle types with skeletal muscle.
- Cardiac structure: branched cells, intercalated discs = desmosomes (hold) + gap junctions (electrically couple → myogenic, coordinated beat)
- Ventricular action potential: phase 0 fast Na⁺, phase 2 plateau from L-type Ca²⁺ current, phase 3 K⁺ repolarisation; long refractory period → no tetanus
- Calcium-induced calcium release (CICR): L-type Ca²⁺ influx triggers SR ryanodine receptors to release more Ca²⁺
- SA-node pacemaker: unstable RMP, funny current (I_f) depolarisation → Ca²⁺-driven upstroke → K⁺ repolarisation; sets heart rate
- Autonomic control: vagus/ACh slows, sympathetic/noradrenaline speeds and strengthens; CO = SV × HR; Starling's law (more filling → more force)
- Smooth-muscle structure: no sarcomeres/striations, dense bodies, caveolae (no T-tubules), unitary (gap-junction-coupled) vs multiunit
It runs across seven topics: Cells & Tissues, Cell Structure & Function, the Special Topics (early development and protein structure), then the exam block — Cell Processes (membrane transport), Blood & the Immune System, Excitable Tissue: Neurons and Excitable Tissue: Muscle. Assessment is split into a theory component and a practical component.
The final examination is worth 40%, sat in the University of Auckland Semester 1 exam period — it is in-person, invigilated and on paper as Teleform multiple-choice (one best answer, no option E/5), not a digital/Inspera exam, and it covers only the second half of the course (Topics 4–7).
A 30% mid-semester test (also paper Teleform MCQ) covers Topics 1–3, laboratories are worth 20%, and online feedback quizzes 10%. A double hurdle applies: you must pass the theory component (at least 40 of the 80 theory marks, combining the test, exam and quizzes with carry-forward) and the practical component separately — and you cannot pass the course if you miss more than two graded labs.
There is no single prescribed textbook; the examinable content is the lecture material, and Tortora & Derrickson is recommended rather than required. Confirm the exact exam date, permitted materials and the current reading list on Canvas and the University of Auckland exam timetable.
Worked example · free
The signature Section C item — the Nernst equilibrium potential
- +1Write the Nernst equation for a monovalent cation (z = +1) at body temperature: E_ion = 61.5 mV × log₁₀([ion]ₒ/[ion]ᵢ). This gives the membrane potential at which net flow of that one ion is zero (electrical pull balances the concentration gradient).
- +1Substitute the sodium concentrations: E_Na = 61.5 × log₁₀(200/10) = 61.5 × log₁₀(20). Since log₁₀(20) ≈ 1.301, E_Na ≈ 61.5 × 1.301 ≈ +80 mV.
- +1Interpret the sign: E_Na is strongly positive (≈ +80 mV), far from the resting potential (≈ −65 mV). At rest the inside is much more negative than E_Na, so both the concentration gradient (high Na⁺ outside) and the electrical gradient (inside negative) drive Na⁺ inward — exactly the inward rush that depolarises the cell when voltage-gated Na⁺ channels open.
Key terms
- Theory hurdle
- The rule that you must earn at least 40 of the 80 theory marks — combining the 30% mid-semester test, the 40% final exam and the 10% online feedback quizzes, with carry-forward across those pieces — to pass BIOSCI 107. Failing the test alone does not fail the course, but the theory total must clear the hurdle, and the practical component must be passed separately.
- Teleform (paper MCQ)
- The optical mark-reader answer sheet the mid-semester test and final exam are sat on — in-person, invigilated and on paper. Questions are multiple-choice with one best answer and no option E/5; the exam is not delivered on Inspera in the current offering. Confirm permitted materials (e.g. a calculator for the Neurons section) on Canvas.
- Nernst equation
- E_ion = 61.5 mV × log₁₀([ion]ₒ/[ion]ᵢ) at body temperature for a monovalent cation — the membrane potential at which net movement of a single ion is zero. Gives E_K ≈ −80 mV and E_Na ≈ +60 to +80 mV depending on the concentrations. Applies only when the membrane is permeable to that one ion.
- Cross-bridge cycle
- The four-step ATP-driven cycle by which a myosin head binds actin, executes a power stroke, detaches when new ATP binds, and re-cocks — sliding the thin filament over the thick. It runs only while cytosolic Ca²⁺ is high enough for troponin to shift tropomyosin off actin's myosin-binding sites; no ATP means no detachment (rigor).
- MHC restriction
- The requirement that a T cell recognises a foreign peptide only when it is displayed on a self-MHC molecule. MHC class I (on all nucleated cells) presents intracellular/viral peptides to CD8⁺ cytotoxic T cells; MHC class II (on professional antigen-presenting cells) presents extracellular/bacterial peptides to CD4⁺ helper T cells.
- CFTR
- The cystic-fibrosis transmembrane conductance regulator — an apical chloride channel gated open by phosphorylation of its R domain plus ATP binding at its nucleotide-binding domains. It is a channel, not a primary active pump. Over-activation by cholera toxin (via cAMP) causes secretory diarrhoea; loss-of-function causes cystic fibrosis.
BIOSCI 107 FAQ
Is BIOSCI 107 hard?
It is broad rather than deep: the challenge is the sheer volume of mechanisms across seven topics, plus one quantitative island — the Neurons section (exam Section C), where you calculate resting and equilibrium potentials with the Nernst and Goldman equations.
Most students find the biology conceptual and manageable if they keep pace, because the assessment is entirely multiple-choice on Teleform and rewards precise recall of mechanisms (which junction uses which protein, which MHC class talks to which T cell, why cardiac muscle can't tetanise).
The two real pressure points are the double hurdle — you must pass theory and practical separately — and not missing more than two graded labs. Keep the weekly quiz rhythm, do not fall behind on the mechanisms, and drill the Nernst/Goldman arithmetic, and it is very passable. Grades sit on the University of Auckland 9-level GPA (A+ down to C−, then D and marginal fail).
Can AI help me with BIOSCI 107?
Yes, as a study aid. Sia is an AI tutor that explains how BIOSCI 107 is actually taught and assessed at the University of Auckland — it will walk the cross-bridge cycle step by step, re-run a Goldman-equation calculation with your numbers, contrast MHC class I and II until it clicks, and check your reasoning on practice questions.
What it will not do is sit graded assessment for you: BIOSCI 107 uses a two-lane academic-integrity policy, and the mid-semester test, final exam and controlled labs are AI-free lanes where AI tools and communicating with anyone are banned. Use Sia to prepare before test night, treat pre-lab quizzes and Lab 4 as the AI-permitted lane, and follow the University of Auckland academic-integrity rules and your course outline.
It explains and drills; it never does your assessment for you.
Where can I find past exam papers / practice for BIOSCI 107?
The course releases practice material on Canvas — a practice mid-semester test, practice exams (2020–2024 scripts appear in the course resources), the Study Questions with worked Nernst/Goldman answers, a practice Teleform answer sheet, plus weekly online feedback quizzes and two PeerWise question-writing tasks.
This guide adds a full set of original worked problems in the same Teleform MCQ pattern — the Nernst/Goldman calculations, the cross-bridge cycle, MHC restriction and more — solved step by step. Because official answer keys are not always published, confirm any answer against the released keys and lecture material on Canvas, and ask Sia to generate fresh practice items in the same style for any topic.
How does the theory-and-practical hurdle work in BIOSCI 107?
There are two hurdles you must clear separately. For the theory component you need at least 40 of the 80 theory marks — that pool is the 30% mid-semester test + 40% final exam + 10% online feedback quizzes, with carry-forward across those pieces, so a weak test alone will not fail you if the exam recovers it.
For the practical component you must pass the labs on their own, and you cannot pass the course if you miss more than two graded labs (lab coat and safety glasses required to attend). Both hurdles must be cleared to pass. If illness or misadventure hits an assessment, apply for aegrotat/compassionate consideration within the stated window with evidence — confirm the exact rules and dates on Canvas and your course outline.
What does the BIOSCI 107 final exam cover, and is it on Inspera?
The final exam is 40% of the course and covers only the second half — Topics 4–7 (membrane transport, blood & immunity, neurons, muscle), organised into four sections: A Blood & Immune, B Cell Processes, C Neurons and D Muscle. It is in-person, invigilated and on paper as Teleform multiple-choice — not an Inspera/digital exam in the current offering (an older 2022 sitting used Inspera, but recent years reverted to paper).
It runs about 2 hours for roughly 90 marks, one best answer per question, no option E/5. The mid-semester test covers Topics 1–3 separately. Confirm the exact date, mark total and permitted materials on Canvas and the University of Auckland exam timetable — the exam sits in the Semester 1 exam period (around June 2027 for the S1 2027 offering).
Questions students ask in each BIOSCI 107 chapter
- How do I keep the cell junctions straight for the test?
- Anchor each junction to its linker protein and its job. Tight junction = occludin/claudin, seals and controls the paracellular gap. Adherens = cadherin to actin, resists tension. Desmosome = cadherin to keratin, resists shear (skin, heart). Hemidesmosome = integrin to laminin, anchors the sheet to the basement membrane. Gap junction = connexins forming a connexon, passes small molecules between cells. The high-yield distinction is that only the hemidesmosome uses integrin (cell-to-matrix); the others that link cells use cadherin. Chapter 01 · Cells, Tissues & Body Organisation
- How many ATP does one glucose really make?
- Use ~30–32 ATP per glucose — that is the figure BIOSCI 107 teaches. Older textbooks quote 36–38, but the course uses the lower, more accurate value that accounts for the cost of importing ADP/Pi and shuttling electrons. Break it down as glycolysis +2, citric-acid cycle +2 (substrate-level), and oxidative phosphorylation ~26–28 (the bulk). Pyruvate oxidation makes 0 ATP directly but feeds NADH into the chain. Chapter 02 · Cell Structure & Cellular Respiration
- What is the difference between a GPCR and a ligand-gated ion channel?
- Both are membrane receptors for water-soluble ligands, but they act on very different timescales. A ligand-gated ion channel opens a pore directly when the ligand binds — fast, ionic and with no amplification, ideal for nerve and muscle signalling. A GPCR does not itself carry ions: it activates a G protein, which activates an enzyme, which generates a second messenger and a phosphorylation cascade — slower but massively amplified, and with several points to regulate. Learn which ligands use which (steroids, being lipid-soluble, use neither — they cross the membrane to cytoplasmic/nuclear receptors). Chapter 03 · Cell Communication & Signalling
- How do I answer the 'use a codon table' question?
- This recurring test item gives you a template DNA strand and asks you to work forward: transcribe it to mRNA (remember RNA uses uracil and is read 5′→3′), then translate codon by codon using the supplied codon table, comparing wild-type to mutant. Classify the change — silent (same amino acid), missense (different amino acid), nonsense (premature stop), or frameshift (1–2 nt indel) — and predict the effect on the protein. The table is always provided, so the skill is doing the decoding carefully and getting the reading frame right, not memorising codons. Chapter 04 · Gene Expression, Cell Division & Cancer
- How do I remember which germ layer makes what?
- Anchor the two easy hooks first: ectoderm makes what covers you and connects you (epidermis and ALL nervous tissue), and endoderm makes the linings of your inner tubes (gut and respiratory epithelium, plus liver and pancreas). Mesoderm is 'everything in the middle that moves or supports' — all muscle, the cardiovascular system, skeleton, kidney and gonads. Then remember they all derive from the epiblast, a common 'which is true about gastrulation' answer. Chapter 05 · Early Development & Protein Structure
- Is CFTR a pump or a channel?
- A channel — this is the exam's favourite catch. CFTR is a chloride channel gated open by phosphorylation of its R domain plus ATP binding at its nucleotide-binding domains. It does not hydrolyse ATP to pump Cl⁻ against a gradient the way a primary active pump would; Cl⁻ moves through it down its electrochemical gradient once the gate is open. The ATP here is a gating signal, not the energy source for uphill transport. Chapter 06 · Membrane Transport & Epithelial Function
- How do I keep MHC class I and II straight?
- Use two hooks. First the numbers: MHC I pairs with CD8 (I × 8) and MHC II pairs with CD4 (II × 4), and each product is 8. Second the antigen source: class I presents peptides made INSIDE the cell (viral) and sits on every nucleated cell, talking to CD8⁺ cytotoxic T cells that kill; class II presents peptides taken in from OUTSIDE (bacterial), sits only on professional antigen-presenting cells, and talks to CD4⁺ helper T cells that coordinate. And remember MHC restriction: a T cell only sees foreign peptide when it is displayed on self-MHC. Chapter 07 · Blood & the Immune System
- When do I use the Nernst equation versus the Goldman equation?
- Use the Nernst equation when only one ion's permeability matters — it gives that ion's equilibrium potential (the voltage at which its net flow is zero), e.g. E_K or E_Na. Use the Goldman equation when several ions contribute at once, as at the real resting potential, because it weights each ion by its permeability. At rest the membrane is far more permeable to K⁺ than Na⁺, so Goldman gives a Vm close to E_K but pulled slightly positive by the small Na⁺ leak. Chapter 08 · Neurons: Membrane Potential & Action Potentials
- Why can one EPSP never fire an action potential?
- Because a single EPSP (~0.1 mV) is tiny compared with the ~15 mV of depolarisation needed to go from rest (~−70 mV) to threshold (~−55 mV). A neuron therefore integrates many inputs: temporal summation adds rapid EPSPs from one synapse before they decay, and spatial summation adds EPSPs from many synapses firing together. Only when the combined depolarisation at the axon initial segment crosses threshold does a spike fire — and inhibitory IPSPs can subtract to prevent it. The neuromuscular junction is the exception: its single end-plate potential is always suprathreshold. Chapter 09 · Synaptic Transmission
- Where exactly does ATP act in the cross-bridge cycle?
- In two places, and neither is the power stroke itself. First, ATP binding to the myosin head causes it to DETACH from actin after the power stroke. Second, hydrolysis of that ATP to ADP + Pi RE-ENERGISES (re-cocks) the head so it can bind again. The power stroke is powered by releasing the ADP + Pi already stored on a cocked head. This is why no ATP means no detachment — the heads stay locked on actin, producing rigor. Chapter 10 · Skeletal Muscle: Contraction & Mechanics
- How is the cardiac calcium trigger different from skeletal muscle?
- In skeletal muscle the trigger is voltage: the muscle's own Na⁺-driven action potential travels down the T-tubules and mechanically opens the SR Ca²⁺-release channels — little external Ca²⁺ is needed. In cardiac muscle the trigger is Ca²⁺ itself: during the plateau, Ca²⁺ enters through L-type channels, and that incoming Ca²⁺ opens SR ryanodine receptors to release more — calcium-induced calcium release. Both then use troponin, but the way the SR is told to release Ca²⁺ differs, which is a classic exam contrast. Chapter 11 · Cardiac & Smooth Muscle
How to study for the exam
Treat the course as two halves with two exams. Topics 1–3 (Cells & Tissues, Cell Structure & Function, and the development/protein Special Topics) are the whole territory of the 30% mid-semester test; Topics 4–7 (transport, blood & immunity, neurons, muscle) are the 40% final.
Both are Teleform multiple-choice, so the winning skill is precise mechanism recall, not essay writing — build a one-line answer for every fact the lecturers flag (which junction uses cadherin vs integrin, the ~30–32 ATP tally, MHC I→CD8 vs MHC II→CD4, why CFTR is a channel not a pump).
Collect the easy percentage first: the 10% online feedback quizzes are described as the easiest marks in the course, so sit all of them, and protect the 20% practical — attend your own lab stream and never miss more than two graded labs, because that is a hard hurdle.
Give the Neurons section (exam Section C) special drilling: it is the one quantitative topic, so practise the Nernst and Goldman equations until the arithmetic and the hyperpolarise/depolarise interpretation are automatic, using the course's worked Study Questions.
Sit the released practice tests and exams under timed conditions on the Teleform-style sheet — at roughly 1.2 minutes per question there is no time to reason from scratch. In exam week, reduce each topic to its mechanism table and, for Section C, the two membrane-potential formulas. Remember both hurdles — pass theory (≥40/80) and practical separately — and confirm every date and rule on Canvas and your course outline.
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