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:
- Reception: Ligand binds to receptor.
- Transduction: Initial message converted and amplified, often involving membrane proteins and second messengers.
- 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.
- Interphase (G1, S, G2):
- 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.