AP BIOLOGY: Cell-Cell Communication Study Sheet

Cell-Cell Communication

• Local or long-distance communication

  • Local: junctions, paracrine (GF) and synaptic (nerve) signaling

  • Long: endocrine signaling (hormones)

• 3 steps: Reception, Transduction, Response

• Reception

  • Internal: hydrophobic/small ligand goes through membrane and binds to internal receptor

  • External: hydrophilic/large ligand binds to receptor on cell membrane

    • G-protein linked receptors: ligand binds to receptor, receptor binds to G-protein, causes GDP to GTP on G-protein activating it, G-protein releases from receptor and binds to/activates an enzyme, enzyme starts STP, GTP-ase removes GTP to GDP inactivating G-protein

    • Receptor tyrosine kinase: 2 ligands bind to receptors forming dimer and activating each Tyr., each Tyr. takes “p” from ATP and adds it, relay proteins bind to each “p”, activating each protein and starting STP’s

    • Ligand-gated ion channels: ligand from one neuron passes through synapse and binds to gated receptor on another neuron, binding of ligand opens up gate and NA+ ions flow in, ions trigger electrical signal, flow stops when ligand leaves

• Transduction

  • Relay molecules: proteins that relay the ligand message, are activated by shape changes (phosphorylation), keep passing on to other proteins until response is reached

  • Protein kinases: type of relay molecule, transfer “p” from ATP to other PK/relay protein, continue passing until response

    • Protein phosphatases dephosphorylate PK’s to be reused

  • Secondary messengers: small ions/molecules, work in G-protein/RTK pathways

    • cAMP: G-protein activated and activates enzyme, adenylyl cyclase, enzyme converts ATP to cAMP, cAMP activates PK A which phosphorylates other proteins

      • Phosphodiesterase: converts cAMP to AMP after cAMP relays its message

      • Cholera: caused by toxin that cause G-proteins to remain active, tons of cAMP produced, high amounts of salt/water go into intestines

    • CA +: G-protein activated and activates enzyme, phospholipase C which converts PIP2 to DAG and IP3, IP3 opens gated CA+ channels in ER and CA+ released to activate other proteins  

• Response

  • Cytoplasmic or Nuclear response

    • Cytoplasmic enzyme activity: enzyme is told to start/activated 

    • Nuclear gene activation: transcription factor is activated, turns on gene that codes for making of an enzyme

• Signal amplification: the more steps/relay proteins the more amplified the message, making for a larger response

• Response specificity: more steps in pathway make response specific 

• Sensory receptors: sensory receptor cell contain receptors to pick up sugar/salt molecules (stimulus), 

  • STP (caused by sugar binding to receptor) triggers ion gates to release changing receptor potential, potential change cause neurotransmitters to be released (action potential) to adjacent sensory neuron, neuron sends message to the brain

  • Sensory adaptation: sensitivity to a stimulus diminishes over time and less signals are made to the brain

• Faulty relay proteins lead to cancer

  • Proto-oncogenes: code for “ras” proteins that activate transcription factor for cell division

    • Mutated: “ras” is hyperactive even without growth factor, constantly signals cell division (cancer)

  • Tumor-suppressor genes: code for “p53” protein that prevent cell division

    • Mutated: “p53” doesn’t signal transcription factor, protein is not made and cannot block cell division, cell division is uncontrolled (cancer)

• Apoptosis

  • Cell goes through blebbing, scavenger cells digest it

  • Can be triggered internally or externally

    • Internal: ligand activates caspases

    • External: mitochondrial leaks (cytochrome C), nuclear signal

  • Ced-9 usually stops Ced-4 from signally death

    • Death signal brought, ced-9 changes shape allowing ced-4 to activate ced-3

    • Ced-3 activates proteases (digest protein) and nucleases (digest DNA)