AP Biology · Unit 4 · 10–15% of Exam ⚡ SPRINT MODE
Cell Communication
& Cell Cycle
Two interlocking systems: cells talk to coordinate behavior, and a tightly controlled cycle governs when they divide. The most exam-dense question type here is "what happens when step X is mutated?" — trace every disruption through the full pathway.
Reception→Transduction→ResponseGPCR / RTK
cAMP / PhosphorylationNeg. vs Pos. Feedback
S Phase / PMATCheckpoints
Cyclins / CDKsOncogenes / p53
⚡ Quick Glance — All Topics at a Glance
| Topic | Priority | Exam Format | Key Trap / Must-Know |
|---|---|---|---|
| 4.1 Cell Communication | ★★★ | MCQFRQ | Protein hormones NEVER enter the cell; steroid hormones cross freely → intracellular receptor |
| 4.2 Signal Transduction Intro | ★★★ | MCQFRQ | Reception→Transduction→Response; signal amplification via phosphorylation cascade |
| 4.3 Signal Pathways & cAMP | ★★★ | MCQFRQ | cAMP made by adenylyl cyclase (NOT by receptor); GPCR → G protein → adenylyl cyclase → cAMP |
| 4.4 Feedback Mechanisms | ★★★ | MCQFRQ | Positive feedback does NOT maintain homeostasis — it amplifies toward a definitive endpoint |
| 4.5 Cell Cycle & Mitosis | ★★★ | MCQData | DNA replication = S phase (interphase), NOT during mitosis; sister chromatids separate in anaphase |
| 4.6 Cycle Regulation & Cancer | ★★★ | MCQFRQ | Oncogenes = dominant (1 mutant copy); tumor suppressors = recessive (need 2 copies lost) |
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Topic 4.1
Cell Communication
Four Modes of Cell-to-Cell Signaling
| Mode | Distance | Mechanism | AP Examples |
|---|---|---|---|
| Direct Contact | Zero | Surface proteins bind adjacent cell; gap junctions (ions/small molecules) | Immune T-cell recognition; cardiac muscle gap junctions; embryonic induction |
| Paracrine | Local (nearby) | Signal diffuses through extracellular fluid to nearby cells only | Growth factors; histamine; morphogens in development; neurotrophins |
| Synaptic | Synapse (~20 nm) | Neurotransmitter released into synaptic cleft → binds postsynaptic receptor | Acetylcholine (neuromuscular junction); dopamine; serotonin |
| Endocrine | Long (bloodstream) | Hormone secreted into blood → travels to distant target cells with specific receptors | Insulin (pancreas → liver); testosterone; epinephrine (adrenaline) |
Critical: Receptor Location Depends on Signal Chemistry
Hydrophilic Signals — CANNOT Cross Membrane
🔴 Cell Surface Receptors
- Protein/peptide hormones: insulin, glucagon, growth hormone, oxytocin
- Neurotransmitters, most growth factors
- Signal binds surface receptor → conformational change → intracellular cascade begins
- Signal molecule never enters the cell
- Response can be: enzyme activation, gene expression change, secretion, cell division
Hydrophobic Signals — CROSS Membrane Freely
🟡 Intracellular Receptors
- Steroid hormones: testosterone, estrogen, cortisol, aldosterone
- Thyroid hormones (T3, T4): lipid-soluble, intracellular receptor
- Diffuse directly through phospholipid bilayer
- Bind receptor in cytoplasm or nucleus
- Hormone–receptor complex acts as transcription factor → directly alters gene expression
- Longer-lasting response (gene expression) vs. faster surface receptor responses
🎯 Exam Sniper
- MCQ (top hit): "Insulin is a protein hormone. Where does it bind and how does it affect liver cells?" → Binds cell surface receptor (tyrosine kinase receptor) → signal transduction cascade → increased glucose uptake/glycogen synthesis. Insulin does NOT enter the cell
- MCQ: "Testosterone can affect gene expression without a signal transduction cascade. Why?" → Testosterone is a steroid (lipid-soluble) → crosses membrane → binds intracellular receptor → complex acts directly as transcription factor in nucleus
- MCQ: "The same signal molecule causes different responses in different cell types. What determines the response?" → The receptor type and the downstream pathway in each cell type — specificity is determined by the receptor, not the signal
💣 Trap Alert
- ❌ Protein hormones (insulin, glucagon, growth hormone) NEVER enter the cell — they bind surface receptors only. Only lipid-soluble signals (steroids, thyroid hormones) cross the membrane
- ❌ Gap junctions allow passage of small molecules/ions between adjacent cells — they are NOT involved in long-distance hormone signaling
- ❌ Signal specificity = determined by the receptor, not the signal molecule itself. Epinephrine can cause different responses in heart vs. liver because they have different receptor subtypes
Topics 4.2–4.3
Signal Transduction Pathways
The Universal Three-Stage Framework
Every Signal Transduction Pathway Follows This Structure
RECEPTION
Ligand binds receptor → conformational change
→
TRANSDUCTION
Relay cascade: G protein / RTK / 2nd messengers / phosphorylation
→
RESPONSE
Gene expression, enzyme activation, secretion, apoptosis, cell division
Three Major Receptor Types
| Receptor Type | How It Works | 2nd Messenger? | Key Examples |
|---|---|---|---|
| G Protein-Coupled Receptor (GPCR) | Ligand binds → activates G protein (GDP→GTP) → G protein activates/inhibits adenylyl cyclase → adenylyl cyclase converts ATP → cAMP → activates PKA (protein kinase A) → phosphorylation cascade | ✅ cAMP | Epinephrine (fight-or-flight); glucagon; olfactory receptors; many drug targets |
| Receptor Tyrosine Kinase (RTK) | Ligand binding → receptor dimerizes → autophosphorylation of tyrosine residues → docking sites for relay proteins → multiple pathways activated simultaneously | ❌ (direct phosphorylation) | Insulin receptor; growth factor receptors (EGF, PDGF); mutated RTKs → cancer |
| Ligand-Gated Ion Channels | Ligand binds → channel opens → specific ions flow down gradient → rapid change in membrane potential | ❌ (ion flux) | Acetylcholine receptor at neuromuscular junction; GABA receptors (inhibitory) |
GPCR / cAMP Pathway — Most Tested
🔁 The cAMP Cascade (Step-by-Step)
- 1. Ligand (e.g., epinephrine) binds GPCR
- 2. G protein activated (GDP replaced by GTP)
- 3. Active G protein activates adenylyl cyclase
- 4. Adenylyl cyclase converts ATP → cAMP (second messenger)
- 5. cAMP activates Protein Kinase A (PKA)
- 6. PKA phosphorylates target proteins → cellular response
- Termination: phosphodiesterase degrades cAMP → signal off
- cAMP is made by adenylyl cyclase, NOT the receptor
Signal Amplification
📡 Why One Signal = Big Response
- Each step activates many molecules of the next step
- One activated receptor → many G proteins → many adenylyl cyclase molecules → huge cAMP production → thousands of PKA activations
- Result: a single hormone molecule can trigger massive cellular response
- This is why hormones are effective at very low concentrations (nanomolar range)
- Phosphorylation cascades: kinase A activates kinase B activates kinase C → amplification at each step
Cellular Responses
🎯 What Signal Pathways Can Trigger
- Gene expression: phosphorylated transcription factors enter nucleus → activate/repress genes
- Enzyme activation/inhibition: phosphorylation changes enzyme shape/activity
- Secretion: vesicle exocytosis triggered (e.g., neurotransmitter release)
- Cell division: growth factor → RTK → cascade → CDK activation
- Apoptosis: programmed cell death initiated by death ligands
🎯 Exam Sniper
- FRQ (very common): "Epinephrine binds to liver cells, causing glycogen breakdown. Trace the signal from reception to response." → GPCR binding → G protein activation → adenylyl cyclase → cAMP → PKA → phosphorylates glycogen phosphorylase → glycogen → glucose. Must name all steps
- MCQ (mutation scenario): "A mutation keeps the G protein permanently bound to GTP. What is the most likely effect?" → Adenylyl cyclase is permanently active → cAMP never stops → PKA always active → uncontrolled cellular response (possible uncontrolled division = cancer)
- MCQ: "Why can a small amount of hormone produce a large cellular effect?" → Signal amplification — each step in the cascade activates many molecules of the next protein, exponentially multiplying the response
- MCQ: "A drug inhibits phosphodiesterase. What would happen to cAMP levels?" → cAMP levels would increase (phosphodiesterase normally degrades cAMP; blocking it prolongs the signal). This is how caffeine and Viagra work!
💣 Trap Alert
- ❌ cAMP is produced by adenylyl cyclase, NOT by the receptor or the G protein directly. The pathway is receptor → G protein → adenylyl cyclase → cAMP (3 steps before cAMP appears)
- ❌ RTKs do NOT use cAMP as a second messenger — they directly phosphorylate tyrosine residues and dock relay proteins
- ❌ The ligand itself is the first messenger; cAMP is the second messenger — it carries the signal inside the cell
A researcher discovers a mutation in the gene encoding adenylyl cyclase that causes the enzyme to be constitutively active (always "on") even without a G protein signal. Which of the following best describes the likely consequence of this mutation?
- (A) Cells would stop responding to all signals because the normal signaling pathway is bypassed
- (B) cAMP would be continuously produced, leading to persistent activation of PKA and uncontrolled downstream responses
- (C) The G protein would remain permanently inactive because adenylyl cyclase no longer requires its activation
- (D) Cells would become resistant to ligand binding because surface receptors would be downregulated
Answer: (B) — Adenylyl cyclase normally converts ATP to cAMP only when activated by an active G protein. If it is constitutively active, it continuously produces cAMP regardless of whether a ligand is present. This keeps PKA permanently active, which continuously phosphorylates downstream targets. Depending on the cell type, this could mean uncontrolled gene expression, metabolic changes, or uncontrolled cell division. This type of "stuck-on" mutation in a signaling component is a common mechanism of oncogenesis (cancer).
Topic 4.4
Feedback Mechanisms
🔵 Negative Feedback — Maintains Homeostasis
- Output opposes the original stimulus
- Keeps system near a set point
- Most common regulatory mechanism in biology
- Examples:
- Blood glucose ↑ → insulin released → glucose uptake ↑ → blood glucose ↓ (back to normal)
- Body temp ↑ → sweating/vasodilation → heat loss → temp ↓
- Thyroid axis: TRH → TSH → T3/T4 → T3/T4 inhibits TRH + TSH (feedback loop)
- Enzyme feedback inhibition (Unit 3): end product inhibits first enzyme → stops overproduction
🟠 Positive Feedback — Amplifies Toward Endpoint
- Output amplifies the original stimulus
- Does NOT maintain homeostasis — moves away from set point
- Always drives toward a definitive, self-limiting endpoint
- Examples:
- Childbirth: oxytocin → contractions → more oxytocin → more contractions → birth (ends feedback)
- Blood clotting: clot activates more clotting factors → faster clot formation → seals wound (ends it)
- Action potential: Na⁺ channels open → depolarization → more Na⁺ channels open → full spike
- LH surge: estrogen → LH release → more estrogen → ovulation (definitive endpoint)
🎯 Exam Sniper
- MCQ (classic): "Which mechanism maintains blood glucose at a stable level?" → Negative feedback (insulin + glucagon form opposing loops around the set point)
- MCQ: "During childbirth, uterine contractions stimulate more oxytocin release, which causes more contractions. This is an example of..." → Positive feedback — note that it ends when the baby is born (definitive endpoint reached)
- FRQ: "Explain the role of negative feedback in regulating thyroid hormone levels." → Hypothalamus releases TRH → pituitary releases TSH → thyroid releases T3/T4 → high T3/T4 inhibits hypothalamus AND pituitary → TRH and TSH decrease → T3/T4 production decreases → returns to set point
- MCQ: "A patient has a tumor that continuously secretes cortisol. How does this affect CRH and ACTH levels?" → Negative feedback: high cortisol → suppresses hypothalamus (↓ CRH) and pituitary (↓ ACTH) — both would decrease
💣 Trap Alert
- ❌ Positive feedback does NOT maintain homeostasis — it deliberately amplifies a signal away from the set point. Only negative feedback maintains a stable set point
- ❌ Positive feedback always has a built-in definitive endpoint — birth, wound sealed, ovulation — after which the loop naturally terminates
- ❌ Enzyme feedback inhibition (Unit 3) = negative feedback — end product inhibits an earlier step, preventing overproduction. Don't confuse with positive feedback
Topic 4.5
The Cell Cycle & Mitosis
Cell Cycle Phases — Know What Happens in Each
G₁
Gap 1 / Growth
Cell grows; produces proteins/organelles; receives signals to divide or not. Restriction point here — commit to division or enter G₀.
S Phase
DNA Synthesis
DNA replication occurs here — NOT during mitosis. Each chromosome → 2 identical sister chromatids joined at centromere. DNA content doubles (2N → 4N).
G₂
Gap 2 / Prep
Cell grows more; synthesizes proteins for division (tubulin for spindle); checks DNA replication is complete before entering mitosis.
Mitosis
PMAT
Nuclear division — 4 stages: Prophase, Metaphase, Anaphase, Telophase. Sister chromatids separate. Produces 2 genetically identical nuclei.
Cytokinesis
Cell Division
Cytoplasm divides. Animals: cleavage furrow (actin contracts). Plants: cell plate forms (vesicles fuse). Produces 2 daughter cells.
G₀
Non-Dividing
Cells exit cycle. Neurons, muscle cells remain here permanently. Liver cells can re-enter G₁ if stimulated. NOT the same as dead.
Mitosis Phases — PMAT Table
| Phase | Key Events | AP Exam Identifier |
|---|---|---|
| Prophase | Chromatin condenses into visible chromosomes; nuclear envelope breaks down; spindle fibers form from centrioles (animals) | Chromosomes visible but NOT yet aligned; nuclear envelope gone |
| Metaphase | Chromosomes align at metaphase plate (cell equator); spindle fibers attach to centromeres (kinetochores) of both sister chromatids | Chromosomes lined up in middle — easiest phase to count chromosomes |
| Anaphase | Sister chromatids pulled apart to opposite poles; centromeres split; cell elongates | Chromosomes moving to poles in a "V" shape; cell looks stretched |
| Telophase | Nuclear envelopes reform around each set of chromosomes; chromosomes decondense; spindle breaks down | Two nuclei forming; chromosomes becoming less visible |
🎯 Exam Sniper
- MCQ (data): "A bar graph shows the percentage of cells in each cell cycle phase. Which phase would normally have the highest percentage?" → G₁ (cells spend most time here, and many cells may be in G₀)
- MCQ: "A drug prevents spindle fiber formation. At which phase would cells be arrested?" → Metaphase (can't attach to kinetochores → can't move to anaphase). This is how Taxol/paclitaxel works as a cancer drug
- MCQ: "When does DNA replication occur?" → S phase of interphase — BEFORE mitosis begins. By prophase, DNA is already fully replicated
- Data Analysis: Given a graph of DNA content vs. time, identify: flat at 2N = G₁ or G₂; rising from 2N to 4N = S phase; flat at 4N = G₂; dropping to 2N = end of mitosis/cytokinesis
💣 Trap Alert
- ❌ DNA replication occurs in S phase (interphase), NOT during mitosis. By the time prophase starts, all DNA is already copied
- ❌ Sister chromatids separate in mitosis anaphase AND meiosis II anaphase. In meiosis I anaphase, homologous chromosomes separate (sister chromatids stay together) — this distinction is tested heavily
- ❌ G₀ is not cell death — it's a non-dividing but metabolically active state. Neurons are in G₀ permanently
- ❌ Plants do NOT have centrioles during mitosis — they still form a mitotic spindle from other structures (MTOCs)
Topic 4.6
Cell Cycle Regulation & Cancer
Molecular Drivers
⚙️ Cyclins & CDKs
- CDKs (Cyclin-Dependent Kinases): enzymes that drive cell cycle transitions by phosphorylating target proteins
- Cyclins: regulatory proteins that activate CDKs; their concentration rises and falls during the cycle (hence "cyclin")
- Cyclin + CDK complex → active kinase → cell cycle advances
- When cyclin is degraded → CDK inactivated → checkpoint enforced
- Different cyclin–CDK pairs control different transitions (G₁→S, G₂→M, etc.)
Quality Control
🛑 The Three Checkpoints
- G₁ Checkpoint (restriction point): Is the cell large enough? Is DNA undamaged? Are growth signals present? → Pass → enter S phase; fail → G₀ or apoptosis
- G₂ Checkpoint: Was DNA replicated completely and correctly? Are conditions suitable? → Pass → enter mitosis
- Spindle Checkpoint (M checkpoint): Are ALL kinetochores attached to spindle fibers? → Pass → anaphase begins; fail → wait (prevents chromosome loss)
Guardian of the Genome
🛡 p53 Tumor Suppressor
- p53 = transcription factor; activated by DNA damage
- Halts cycle at G₁ checkpoint → allows time for DNA repair
- If damage unrepairable → p53 triggers apoptosis (programmed cell death)
- p53 gene mutated in ~50% of all human cancers
- Called "guardian of the genome" — prevents damaged cells from dividing
- p53 is a tumor suppressor — loss of function promotes cancer
Oncogenes vs. Tumor Suppressors — Most Tested Cancer Concept
🔴 Oncogenes (Accelerator Stuck On)
- Derived from proto-oncogenes (normal genes promoting cell division)
- Mutation → gain of function → protein always active even without signal
- Dominant: only ONE mutant copy needed to promote cancer
- Examples: mutant Ras (G protein always on); mutant RTK (always phosphorylating); amplified growth factor receptors
- Analogy: stuck accelerator — cell divides regardless of signals
- Most common mechanism: point mutation, gene amplification, chromosomal translocation
🔵 Tumor Suppressor Genes (Brakes Removed)
- Normal proteins that inhibit cell division or promote apoptosis
- Mutation → loss of function → no longer restrains cell cycle
- Recessive: BOTH copies must be lost for cancer (two-hit hypothesis)
- Examples: p53 (halts cycle + triggers apoptosis on DNA damage); Rb (retinoblastoma protein — blocks G₁→S until conditions right)
- Analogy: cut brake lines — cell can't stop dividing
- Hereditary cancers often involve one inherited mutant copy + one somatic mutation
Programmed Cell Death
💀 Apoptosis vs. Necrosis
- Apoptosis: ordered, energy-requiring, no inflammation; cell shrinks; fragments phagocytosed cleanly; healthy and necessary
- Functions: embryonic development (finger separation), immune cell selection, cancer surveillance, removal of damaged cells
- Necrosis: accidental cell death from injury/infection; membrane ruptures; cell contents spill → inflammatory response
- Key distinction: apoptosis never causes inflammation
Cancer = Loss of Both Controls
⚠️ How Cancer Develops
- Cancer requires MULTIPLE mutations over time
- Need: activation of proto-oncogene(s) AND loss of tumor suppressor(s)
- Cells divide uncontrollably + evade apoptosis + ignore checkpoints
- Metastasis: cells detach, invade basement membrane, enter bloodstream, colonize distant organs
- Mutations can be: inherited, spontaneous, induced by carcinogens (UV, chemicals, viruses)
🎯 Exam Sniper
- FRQ (most common Unit 4 FRQ): "A mutation causes the Ras G protein to remain permanently active. Explain how this leads to uncontrolled cell division." → Ras is normally activated briefly by RTK → activates downstream kinases → cell division. Permanently active Ras → signal cascade never stops → transcription factors for division always active → cell divides without growth factor signal
- MCQ: "A person inherits one defective copy of the p53 gene. They have not yet developed cancer. Why?" → p53 is a tumor suppressor (recessive) — both copies must be lost (two-hit hypothesis). One functional copy provides sufficient tumor suppression
- MCQ: "Which of the following represents the effect of a tumor suppressor gene mutation?" → Loss of function → cell cycle proceeds without proper checkpoint monitoring → uncontrolled division
- MCQ: "During the M checkpoint, all kinetochores must be attached to spindle fibers before anaphase begins. What is the consequence of this checkpoint failing?" → Chromosomes may not separate equally → daughter cells receive abnormal chromosome numbers (aneuploidy) → possibly cancer or cell death
Two types of mutations are frequently found in cancer cells: (1) a mutation that causes the epidermal growth factor receptor (EGFR) to be continuously active without ligand binding, and (2) a mutation that inactivates both copies of the Rb gene. How does each mutation contribute to uncontrolled cell division?
- (A) Both are recessive tumor suppressor mutations that eliminate growth inhibition signals
- (B) Both are dominant oncogene mutations that continuously stimulate division
- (C) EGFR mutation is a dominant oncogene (gain of function); Rb mutation is a recessive tumor suppressor loss (loss of function) — together they remove both brakes and accelerators
- (D) EGFR mutation prevents apoptosis; Rb mutation activates CDK-independent cell division
Answer: (C) — EGFR is a receptor tyrosine kinase (proto-oncogene). The mutation causes it to signal continuously → growth signal cascade always on → cell division stimulated without ligand (dominant gain-of-function oncogene — one mutant copy is enough). Rb is a tumor suppressor — it normally blocks G₁→S transition until conditions are right. Losing BOTH copies of Rb removes this brake → cell enters S phase uncontrollably (recessive loss-of-function — both copies must be lost). Cancer typically requires losing BOTH types of controls: gaining an oncogene AND losing tumor suppressors.
Practice
Sprint Practice — Mixed Questions
After a meal, blood glucose rises. The pancreas responds by secreting insulin, which causes liver and muscle cells to take up glucose, returning blood glucose to normal. A person has a mutation that prevents the production of functional insulin receptors on liver cells. What is the most likely outcome?
- (A) Blood glucose would remain normal because glucagon would compensate
- (B) Blood glucose would remain elevated because liver cells cannot respond to insulin's signal
- (C) Insulin production would increase because the pancreas compensates for liver cell insensitivity
- (D) Liver cells would take up more glucose through facilitated diffusion to compensate
Answer: (B) — Insulin is a hydrophilic protein hormone that cannot cross the plasma membrane. It must bind surface receptors on target cells to initiate the signal transduction cascade leading to glucose uptake. If liver cells have non-functional insulin receptors, the signal cannot be received, no transduction cascade occurs, and glucose transporters (GLUT4) are not activated → blood glucose stays elevated. This is the molecular basis of type 2 diabetes (insulin resistance). Note: (C) is partly true as a compensation mechanism, but the primary direct outcome is elevated blood glucose.
A researcher uses flow cytometry to measure the DNA content per cell in a rapidly dividing cell population. She finds: 30% of cells have DNA content = 2N; 15% have DNA content between 2N and 4N; 50% have DNA content = 4N; 5% have DNA content dropping from 4N to 2N. Which phases do each population correspond to?
- (A) 2N = G₁ (or G₀); 2N–4N = S phase; 4N = G₂ + mitosis; dropping = cytokinesis/late anaphase-telophase
- (B) 2N = Prophase; 2N–4N = Metaphase; 4N = Anaphase; dropping = Telophase
- (C) 2N = S phase; 2N–4N = G₁; 4N = G₂ only; dropping = G₁ re-entry
- (D) 2N = Mitosis; 4N = Interphase; dropping = apoptosis
Answer: (A) — DNA content is the key: G₁ cells have undergone no replication → 2N. S phase cells are actively replicating → DNA content rises from 2N to 4N (variable). G₂ and mitotic cells (pre-cytokinesis) have completed replication → 4N. Late mitosis/cytokinesis separates the 4N into two 2N cells → DNA content drops back to 2N. The 50% at 4N includes both G₂ and all mitotic stages (prophase through late telophase). This is a standard flow cytometry interpretation question.
⚠ Trap Alert
Unit 4 High-Frequency Exam Traps
- 📡Protein hormones NEVER enter the cell — they bind surface receptors onlyInsulin, glucagon, growth hormone, oxytocin — all too large and hydrophilic to cross the membrane. They bind cell surface receptors and initiate signal cascades from outside. Only lipid-soluble signals (steroids, thyroid hormones) cross the membrane to bind intracellular receptors.
- 🧪cAMP is produced by adenylyl cyclase — NOT by the receptor or G protein directlyThe order is: Ligand → GPCR → G protein (GDP→GTP) → G protein activates adenylyl cyclase → adenylyl cyclase converts ATP to cAMP → cAMP activates PKA. Three relay steps before cAMP appears. A common wrong answer is "receptor produces cAMP."
- 🔁Positive feedback does NOT maintain homeostasisPositive feedback amplifies a signal AWAY from the set point toward a definitive endpoint (childbirth, clot formation, action potential). Only negative feedback maintains homeostasis by opposing deviations. This distinction is one of the most consistently tested concepts in Unit 4.
- 🧬DNA replication occurs in S phase — NOT during mitosisBy the time prophase begins, DNA is already fully replicated. Each chromosome consists of 2 identical sister chromatids joined at the centromere. Mitosis only separates pre-replicated chromosomes. Students who say "DNA replicates during mitosis" lose points every time.
- 🔀Sister chromatids separate in Anaphase of MITOSIS — homologs separate in Meiosis I AnaphaseIn mitosis anaphase: sister chromatids separate → each daughter gets one copy of each chromosome. In meiosis I anaphase: homologous chromosome pairs separate (sister chromatids stay attached). In meiosis II anaphase: sister chromatids finally separate (like mitosis). This is heavily tested in genetics questions.
- 🎯Oncogenes = dominant (1 copy); Tumor suppressors = recessive (need 2 copies lost)Proto-oncogene → oncogene = gain-of-function mutation → one mutant copy is enough to continuously drive division (dominant). Tumor suppressor loss = loss-of-function → both copies must be inactivated before the brake is fully removed (recessive, two-hit hypothesis). Hereditary cancer syndromes often involve one inherited mutant suppressor copy + one somatic mutation to the second copy.
- 💀Apoptosis does NOT cause inflammation — necrosis doesApoptosis = ordered, programmed cell death; cell shrinks and fragments; phagocytes clean up debris; no inflammatory response. This is healthy and necessary (embryogenesis, immune selection, removal of DNA-damaged cells). Necrosis = uncontrolled cell death from injury; membrane ruptures; contents spill → inflammatory response. Never say "apoptosis causes inflammation."
✓ Last-Min Checklist
Pre-Exam 10-Minute Checklist
Click each item to check off. Review any you can't confirm.
Cell Communication & Signal Transduction (4.1–4.3)
- Protein hormones (hydrophilic) → surface receptor → signal cascade; steroid hormones (hydrophobic) → cross membrane → intracellular receptor → transcription factor
- Signal specificity is determined by the RECEPTOR type, not the signal molecule
- Three stages of every pathway: Reception → Transduction → Response
- GPCR pathway: Ligand → GPCR → G protein → adenylyl cyclase → cAMP → PKA → response
- RTK: ligand → dimerization → autophosphorylation → multiple pathways; no cAMP
- Signal amplification: one ligand → massive response (each cascade step activates many molecules of the next)
- Phosphodiesterase degrades cAMP → terminates signal; inhibiting it prolongs signal
Feedback Mechanisms (4.4)
- Negative feedback: opposes stimulus → maintains homeostasis at set point (blood glucose, temp, hormone axes)
- Positive feedback: amplifies stimulus → drives toward definitive endpoint (childbirth, clotting, action potential)
- Can give at least 2 examples of each type with mechanism
Cell Cycle & Mitosis (4.5)
- Interphase: G₁ (grow) → S (DNA replication) → G₂ (prepare); mitosis + cytokinesis follows
- DNA replication = S phase only — NOT during mitosis
- PMAT: Prophase (condense), Metaphase (align at plate), Anaphase (sister chromatids separate), Telophase (reform nuclei)
- Cytokinesis: cleavage furrow (animals) vs. cell plate (plants)
- G₀ = non-dividing state (neurons permanently; liver can re-enter cycle)
Cycle Regulation & Cancer (4.6)
- Cyclins activate CDKs → drive cycle transitions; cyclin degradation = checkpoint enforcement
- G₁ checkpoint: cell size + DNA integrity + growth signals; G₂: complete replication; M: all kinetochores attached
- p53: activated by DNA damage → halts G₁ → repair or apoptosis; mutated in ~50% of cancers
- Oncogene = dominant gain-of-function (1 copy enough); Tumor suppressor = recessive loss-of-function (both copies needed)
- Apoptosis = ordered, no inflammation, healthy; Necrosis = rupture, inflammation, injury-caused
⚡ Final Sprint Strategy for Unit 4
- Top exam question format: "A mutation causes protein X to be constitutively active/inactive. Trace the consequence through the entire pathway." → Always identify: (1) what the protein normally does, (2) whether the mutation = gain or loss of function, (3) step-by-step downstream effects, (4) final cellular outcome
- Must-master pathways: Full GPCR/cAMP cascade (can write it from memory); negative feedback blood glucose loop (insulin + glucagon); cell cycle with checkpoints labeled
- Cancer FRQ template: Name the gene type (oncogene/tumor suppressor) → explain the normal function → explain how the mutation changes activity → link to uncontrolled cell division
- Connections forward: Signal transduction → Unit 5 (hormone signaling in gene regulation); Cell cycle → Unit 5 (meiosis comparison); Apoptosis → Unit 7 (immunity); Positive/negative feedback → Unit 8 (population ecology feedback loops)