AP Bio Unit 4 Review Flashcards

Cell Communication, Cell Signaling, and Signal Transduction

• Cells communicate constantly, a basic feature of life.
• Cells are in populations or multicellular organisms, not truly isolated.
• Direct cell to cell communication:
  • Junctions between adjacent cells allow molecule passage.
  • Enables one cell to change another's behavior.
• Communication via signals:
  • Cells secrete molecules into the bloodstream or extracellular fluid.
  • Target cells pick up these messages.
  • Signals are called ligands.
  • Two types of ligands:
    • Hormones: Long-distance signals traveling via the bloodstream from glands.
    • Local Regulators: Short-distance cell-to-cell communication.
• Ligands are signaling molecules that bind to receptors based on complementary shape (like enzymes and substrates).
• Binding leads to a cellular response.
• Quorum Sensing:
  • Cell communication in biofilm formation in bacteria (e.g., plaque on teeth).
  • Bacteria release signaling molecules that bind to cytoplasmic receptors.
  • When the signal intensity exceeds a threshold (quorum), genes are activated.
  • Gene activation leads to biofilm production (polysaccharide).
  • Takeaway: All cells communicate, even bacteria, and brush your teeth.
• Cell signaling phases:
  1. Reception: Ligand binds to receptor.
  2. Transduction: Initial message converted and amplified, often involving membrane proteins and second messengers.
  3. Response: Cellular change occurs due to activated enzymes or gene activation.
• Reception Phase:
  • Signal molecule (ligand) binds with the receptor molecule.
  • Binding is based on complementary shape.
  • Receptor is embedded in the cell membrane's phospholipid bilayer.
• Transduction and Response Phases:
  • Receptor interacts with membrane proteins to produce a second messenger.
  • Second messenger and relay molecules carry the message to the cytoplasm.
  • This activates enzymes or the nucleus, leading to gene activation.
• Steroid (Nonpolar) Hormones vs. Water-Soluble Hormones:
  • Nonpolar hormones (e.g., estrogen, testosterone) diffuse through the phospholipid bilayer.
  • They bind with cytoplasmic receptors, forming a receptor-hormone complex.
  • The complex diffuses into the nucleus and acts as a transcription factor, activating genes which then make RNA, which ribosomes create proteins from.
  • Water-soluble hormones bind with receptors and interact with second messengers.
  • Steroid hormone responses are generally slower but longer-lasting, while water-soluble hormone responses are quicker.

Epinephrine and G Protein-Coupled Receptor Systems

• Cellular communication works through three phases.

• Fight or flight response context:

  • Adrenal glands produce epinephrine (adrenaline).
  • Epinephrine acts on the liver to produce glucose that goes into the blood.

• Epinephrine (adrenaline) is a polar, water-soluble hormone that binds at the membrane.

  • Epinephrine's \, structure \, contains \, hydroxyl \, groups \, (polar)

• Epinephrine's effects are widespread but tissue-specific.

• Only tissues with receptors respond, response differs based on tissue types.

• Adaptations during fight or flight:

  • Decreased digestion.
  • Increased heart rate.
  • Pupil dilation.
  • Conversion of glycogen to glucose.
  • Bronchial dilation.

• Epinephrine interacts with liver cells causing them to hydrolyze stored glycogen into glucose monomers.

• Glucose diffuses into the bloodstream, providing energy for fight or flight.

• Off state (before epinephrine):

  • Receptor is unbound.
  • Nearby G protein is inactive, bound to GDP (low energy form).
  • Membrane-embedded enzyme adenylyl cyclase is also in the off state.

• Epinephrine enters the system:

  • Epinephrine binds with a G protein-coupled receptor, causing an allosteric change.
  • Nearby G protein interacts with that part of the receptor, receptors change induces G protein to discharge GDP and bind with GTP (high energy form).
  • G protein is activated.

• G protein bound to GTP:

  • Drifts in the membrane and binds with adenylyl cyclase, activating it.
  • Adenylyl cyclase converts ATP into cyclic AMP (cAMP), the second messenger.
    ATP \rightarrow cyclic \, AMP

• Reception review:

  • Ligand (epinephrine) binds with G protein-coupled receptor.
  • Receptor changes shape on the cytoplasmic side.
  • G protein discharges GDP and binds with GTP, becoming activated.
  • G Protein activates adenylyl cyclase, which converts ATP into cyclic AMP.

• Cellular response:

  • Cyclic AMP activates a chain of relay molecules called kinases (phosphorylation cascade).
  • Kinases are activated by phosphorylation, activating the next in the chain.
  • Signal amplification occurs.
  • One epinephrine molecule leads to millions of enzyme activations.
  • In liver cells, the terminal enzyme glycogen phosphorylase is activated which is responsible for converting glycogen into glucose.

• System Shutdown (after threat):

  • Ligand diffuses away.
  • G protein drops the phosphate, binds to GDP, and becomes inactive.
  • Adenylyl cyclase stops creating cyclic AMP.
  • Kinase phosphorylation stops as protein phosphatases clip off phosphates.
  • Glycogen phosphorylase stops hydrolyzing glycogen, blood glucose normalizes.
    *L Liver cells return to their resting state.

Feedback and Homeostasis

• Homeostasis: Tendency of a living system to maintain internal conditions at a relatively constant, optimal level.
• Feedback: Output of a system is also an input.
  • Maintains homeostasis or accelerates internal changes.
  • Negative feedback maintains homeostasis.
  • Positive feedback accelerates change.
• Set points: The value around which a homeostatic process fluctuates.
• Negative Feedback:
  • Output of the system decreases the system's output.
  • Promotes homeostasis, returning a system to its set point.
  • Example: Home thermostat maintaining temperature at a set point.
• Antagonistic Negative Feedback Loops:
  • Paired systems, one for cooling (air conditioner) and one for heating (furnace).
  • Maintain homeostasis by responding to conditions above or below the set point.
• Blood Sugar Homeostasis:
  • Insulin is the main hormone.
  • Negative feedback system:
    • High blood glucose levels trigger insulin release from the pancreas.
    • Insulin binds at a receptor in the liver, activating a signaling cascade.
    • Glucose transporters open.
    • Glucose diffuses into liver cells and is converted into glycogen or fat.
    • Blood glucose levels decrease, restoring homeostasis.
• Insulin and Glucagon:
  • Blood glucose set point is 90 \frac{mg}{100 \, mL}.
  • Above set point, pancreas releases insulin, glucose is absorbed and stored as glycogen in liver, fat, and muscle cells.
  • Below set point, pancreas releases glucagon, which induces the liver to convert glycogen into glucose.
• Type 2 Diabetes:
  • Cells become insulin resistant.
  • Insulin binding does not lead to the signaling cascade.
  • Glucose channel remains closed.
  • Blood glucose level stays high, damaging organs and tissues.
• Type 1 vs. Type 2 Diabetes:
  • Type 1 (juvenile): Autoimmune disorder where immune cells attack insulin-producing pancreas cells.
  • Type 2 (adult-onset): Insulin resistance where the receptor is insensitive to the insulin signal.
• Positive Feedback:
  • Output of a system increases the system's activity and output.
  • Accelerates biological processes to a conclusion.
  • Childbirth:
    • Baby's growth activates uterine stretch receptors.
    • The brain releases oxytocin.
    • Oxytocin leads to more contraction.
    • Increased contraction leads to more oxytocin release until birth.
  • Fruit Ripening:
    • Ripening leads to the release of ethylene gas.
    • Ethylene induces additional ripening and more ethylene production.
    • Increased ethylene accelerates ripening until all fruit ripens.

The Cell Cycle

• Mitosis duplicates chromosomes, transmitting a cell's entire genome to daughter cells.
• Functions of Mitosis:
  • Growth and repair in multicellular organisms.
  • Reproduction in unicellular eukaryotes.
• Cell Cycle Phases:
  • Interphase (G1, S, G2):
    • G1 (Growth Phase 1): Cell increases in size.
    • S (Synthesis): DNA replication/chromosome duplication.
    • G2 (Growth Phase 2): Growth of structures required for cell division.
  • M Phase (Mitosis): Separation of chromosomes, followed by cytokinesis.
  • Two daughter cells are created that are clones of the parent cell.
  • Phases of Mitosis:
    • Interphase: Cell grows and replicates DNA.
    • Prophase: Chromosomes condense, nuclear membrane disintegrates, spindle apparatus grows.
    • Metaphase: Spindle fibers align chromosomes at the cell equator, doubled chromosomes consist of two sister chromatids.
    • Anaphase: Sister chromatids are pulled apart and dragged to opposite ends of the cell, nonkinetochore microtubules elongate the cell.
    • Telophase: New nuclear membrane grows around each set of chromosomes, chromosomes spread out, nucleolus reappears.
    • Cytokinesis: Cell splits into two daughter cells.
• G0 Phase:
  • Specialized cells (e.g., nerve or muscle cells) leave the cell cycle and enter G0.
  • In G0 cells typically do not divide.
  • Certain stimuli can induce cells in G0 to reenter the cell cycle.

Regulation of the Cell Cycle

• Cell Cycle Checkpoints:
  • Moments when the cell checks internal conditions before progressing to the next phase.
  • If conditions are right, the cell cycle continues; if not, the cell moves into G0 or initiates apoptosis.
  • Primary checkpoints: G1, G2, and M checkpoints.
• Apoptosis (Programmed Cell Death):
  • Signaling cascade involving mitochondria and the nucleus.
  • Highly regulated, unlike traumatic cell injury.
  • Cells are broken down into cytoplasmic fragments (blebs) consumed by immune cells.
• Cyclins and Cyclin-Dependent Kinases (CDKs):
  • Internal regulators of the cell cycle.
  • Cyclins: Molecules whose concentration rises and falls throughout the cell cycle.
  • Cyclin-dependent kinases (CDKs): Kinases that respond to rising and falling cyclin levels.
• Cyclin-CDK Interactions:
  • CDKs are present at a constant level throughout the cell cycle.
  • Cyclin levels rise and fall.
  • High cyclin levels cause cyclins to bind with CDKs to form a complex called maturation (or mitosis) promoting factor (MPF).
  • MPF allows the cell to pass through the G2 checkpoint and divide.
  • During M phase, cyclin is broken down, allowing the process to repeat.
  • Connection Between Cell Division and Cancer:
  • Cancer: Disease of unregulated cell division.
  • Cells become rogue players, pursuing their own destiny at the expense of the organism.
• Genetic Mutations and Cancer:
  • Mutations in proto-oncogenes increase cell division by creating too many growth factors.
  • Mutations in tumor suppressor genes remove cell inhibitors/checkpoints.
  • Cancer occurs when cells have mutated tumor suppressors and overactive growth factors.
• Mutated ROS Proto-Oncogene:
  • Normal ROS (G protein) is only active when an outside growth signal binds with ROS's coupled receptors.
  • Cancerous ROS (oncogene) is constitutively active, binding GTP even without a growth signal.
  • Leads to overproduction of growth factor and too much cell division.
  • Connected with about 30% of human cancers.
• Mutated p53 Tumor Suppressor Gene:
  • Normal Function: DNA damage activates p53, which halts the cell cycle for DNA repair or initiates apoptosis if damage is too great.
  • Mutated p53: Cell continues to divide even with damaged DNA, increasing the chance of acquiring further mutations that can lead to cancer.