AP Biology Unit 4: Cell Communication and Cell Cycle
Unit 4: Cell Communication and Cell Cycle — Quick Review
Signaling Modes
- Direct contact: gap junctions, plasmodesmata
- Paracrine: local (neurotransmitters, growth factors)
- Autocrine: self-signaling
- Endocrine: long-distance via blood (hormones)
Three Stages of Signal Transduction
- Reception — ligand binds receptor
- Transduction — relay through kinase cascade + second messengers
- Response — gene expression or enzyme activity changes
Receptor Types
- GPCRs — largest family; activate G-proteins (GDP → GTP swap)
- RTKs — dimerize, autophosphorylate tyrosines, trigger multiple pathways
- Ligand-gated ion channels — fast, at synapses
- Intracellular receptors — for steroid hormones (lipid-soluble), act as transcription factors
💡 Exam Tip: Steroid hormones are the only ligands that cross the membrane. If a question says "hormone enters cell and binds receptor," it's steroid.
Second Messengers
- cAMP — made by adenylyl cyclase, activates PKA
- Ca²⁺ — muscle contraction, exocytosis
- IP₃/DAG — from PIP₂
Amplification
- One ligand → millions of response molecules (via cascades)
- Classic example: epinephrine → cAMP → glycogen breakdown (Sutherland)
Feedback Loops
- Negative — opposes change, restores set point (insulin/glucose, thermoregulation)
- Positive — amplifies change (childbirth/oxytocin, blood clotting, action potentials)
Cell Cycle Phases
- G₁ — growth
- S — DNA replication
- G₂ — growth, preparation
- M — mitosis + cytokinesis
- Interphase = G₁ + S + G₂ (~90% of cycle)
Mitosis (PMAT)
- Prophase — chromosomes condense, spindle forms
- Metaphase — chromosomes at equator
- Anaphase — sister chromatids separate (cohesin cleaved)
- Telophase — nuclear envelopes reform
- Cytokinesis — cleavage furrow (animal) or cell plate (plant)
Cell Cycle Regulation
- Cyclins oscillate; CDKs are constant but inactive without cyclin
- Cyclin-CDK complex drives progression past checkpoints
Checkpoints
- G₁ — cell size, DNA integrity, growth signals (p53 guards here)
- G₂ — DNA fully replicated?
- M (Spindle) — all chromosomes attached?
Cancer
- Oncogenes = mutated proto-oncogenes = stuck-on gas pedal (e.g., Ras)
- Tumor suppressors = brakes (e.g., p53, Rb); lost in cancer
- Cancer cells ignore density-dependent inhibition and anchorage dependence
- HeLa cells (Henrietta Lacks, 1951) — still dividing
💡 Exam Tip: For any signaling mutation FRQ, ask: stuck ON or stuck OFF? Then trace downstream.
Key Terms
- Ligand — signaling molecule that binds receptor
- GPCR — G-protein coupled receptor
- RTK — receptor tyrosine kinase
- Second messenger — small molecule relaying signal (cAMP, Ca²⁺)
- Kinase — adds phosphate; phosphatase — removes it
- Cyclin / CDK — cell cycle drivers
- p53 — guardian of the genome
- Apoptosis — programmed cell death
- Proto-oncogene / oncogene — normal vs mutated growth driver
- Tumor suppressor — brake gene
Must-Know for the Exam ✅
- Name and distinguish the 4 signaling modes
- Describe the 3 stages of signal transduction with an example
- Compare GPCRs vs RTKs vs intracellular receptors
- Explain how phosphorylation cascades amplify signals
- Give one example each of negative and positive feedback
- List the phases of the cell cycle in order with what happens in each
- Describe the 3 checkpoints and what they monitor
- Explain the role of cyclins and CDKs
- Distinguish oncogenes from tumor suppressors
- Explain how a mutation (e.g., Ras, cholera toxin) disrupts signaling
- Contrast animal vs plant cytokinesis
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