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

  1. Reception — ligand binds receptor
  2. Transduction — relay through kinase cascade + second messengers
  3. 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)

  1. Prophase — chromosomes condense, spindle forms
  2. Metaphase — chromosomes at equator
  3. Anaphase — sister chromatids separate (cohesin cleaved)
  4. Telophase — nuclear envelopes reform
  5. 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