Unit 4: Cell Communication and Cell Cycle
AP Biology: 52 practice questions with detailed explanations.
Unit Study Guide
Executive Summary
Unit 4 covers how cells talk (signal transduction) and how they divide (cell cycle and mitosis). Regulation failures underlie cancer.
Cell communication
Signals may travel directly (gap junctions), locally (paracrine, synaptic), or distantly (endocrine hormones). Reception requires a receptor protein specific for the ligand. Transduction converts the signal into a cascade — often phosphorylation cascades and second messengers like cAMP — amplifying each step. The response is typically gene activation or enzyme activation.
Signal transduction pathways
A receptor changes shape on binding; relay proteins pass the message; second messengers diffuse and amplify; protein kinases phosphorylate targets; phosphatases switch them off. G-protein-coupled receptors and receptor tyrosine kinases are the exam's workhorses.
Changes in pathways
Mutations can lock pathways on (constitutively active) or off. Different cells respond differently to the same ligand because they express different receptors or downstream machinery. Drugs often target receptors or kinases.
Feedback loops
Negative feedback returns a system to set point (blood glucose via insulin/glucagon). Positive feedback amplifies change (oxytocin during labor, ripening fruit's ethylene, blood clotting) — it needs an external reset to stop.
Cell cycle
Interphase: G₁ (growth), S (DNA replication), G₂ (prep). Mitosis: prophase (chromosomes condense, spindle forms), metaphase (chromosomes align at the plate), anaphase (sister chromatids separate), telophase (nuclear envelopes reform), cytokinesis (cytoplasm splits). Result: two genetically identical diploid daughters.
Regulation and cancer
Checkpoints (G₁/S, G₂/M, M) verify conditions before proceeding. Cyclins and cyclin-dependent kinases (Cdks) drive the cycle; p53 halts damaged cells. Cancer arises when checkpoint genes mutate — cells divide without restraint, often aided by loss of density-dependent inhibition and anchorage dependence.