What is the central concept of the Fluid Mosaic Model?
Biological membranes behave as two-dimensional fluids where lipids and proteins can laterally diffuse, creating a dynamic mosaic of phospholipids, cholesterol, proteins, and carbohydrates.
How does cholesterol influence membrane fluidity?
Cholesterol buffers fluidity:
* At high temperatures, → reduces fluidity by restricting phospholipid movement.
* At low temperatures, → prevents tight packing and increases fluidity.
It also reduces membrane permeability to small water-soluble molecules.
What types of membrane proteins exist?
- Integral/transmembrane proteins: Span the bilayer; often α-helical or β-barrel.
- Peripheral proteins: Loosely associated with surfaces via electrostatic interactions or anchoring.
- Lipid-anchored proteins: Covalently attached to lipids (e.g., GPI-anchored).
Why is membrane fluidity biologically important?
Fluidity ensures:
* Proper diffusion of proteins for signal transduction.
* Membrane fusion, budding, and vesicle trafficking.
* Selective permeability and function of transport proteins.
* Dynamic responses to environmental changes (e.g., temperature).
What are glycolipids and glycoproteins, and what is their function?
Proteins or lipids with a carbohydrate attached to their surface; quintessential for cell-cell recognition, which allows cells to determine if a substance is foreign or not.
What are antigens when discussing cell-cell recognition of different blood types, and how do they relate?
Antigens are substances, often proteins or sugars, found on the surface of red blood cells that act as identifying markers, and they determine a person’s blood type. They relate to glycolipids and glycoproteins because they are the ones that identify these markers, and if the blood type donated is incorrectly matched, then major negative side effects will occur.
What two forces together define the membrane potential, and how do they arise?
Membrane potential is the combined result of:
1. Ion concentration gradients (created by pumps like Na⁺/K⁺-ATPase)
2. Selective permeability of the plasma membrane (especially to K⁺ via leak channels)
Define an electrochemical gradient and explain why it is more informative than a concentration gradient alone.
An electrochemical gradient combines:
* Chemical gradient (difference in concentration)
* Electrical gradient (charge difference)
This matters because charged ions move according to net force, not concentration alone.
Why does Na⁺ strongly enter cells when Na⁺ channels open?
- The concentration gradient (high Na⁺ outside)
- The electrical gradient (negative interior)
drive Na⁺ inward → maximal inward force.
What defines primary active transport at the molecular level?
Primary active transport directly couples ATP hydrolysis to:
* A conformational change in a transport protein
* Movement of solute against its electrochemical gradient
Describe the full transport cycle of the Na⁺/K⁺ pump in correct order.
- 3 Na⁺ bind intracellularly
- ATP phosphorylates the pump
- Pump changes conformation → Na⁺ released outside
- 2 K⁺ bind extracellularly
- Dephosphorylation
- Pump returns inward-facing → K⁺ released inside
Why is the Na⁺/K⁺ pump considered electrogenic, and why does this matter?
It is electrogenic because:
* Moves 3 positive charges out
* Moves 2 positive charges in
Net export of positive charge maintains:
* Membrane potential
* Neuronal excitability
* Secondary transport systems
How does secondary active transport differ fundamentally from primary active transport?
Secondary active transport:
* Does not use ATP directly
* Uses the energy stored in an ion gradient (usually Na⁺). Example: Intestinal glucose uptake occurs via secondary active transport using the Na⁺ electrochemical gradient established by the Na⁺/K⁺ ATPase, followed by facilitated diffusion into the bloodstream. * Depends on primary active transport to exist
Why are channel proteins incapable of primary active transport?
Because channels:
* Do not undergo large conformational changes
* Do not bind ATP
* Only allow passive diffusion down gradients
Explain the difference between phagocytosis and pinocytosis, and give a cellular context where each is particularly important.
Phagocytosis: “Cell eating” – the cell engulfs large particles (bacteria, debris) via pseudopodia to form a phagosome. Often performed by immune cells (e.g., macrophages, neutrophils).
* Pinocytosis: “Cell drinking” – the cell takes in extracellular fluid and dissolved solutes through small vesicles. Important for nutrient uptake in epithelial cells.
* Key distinction: particle size (large vs. small), and type of cargo (particulate vs. fluid).
Predict what might happen to a cell’s homeostasis if receptor-mediated endocytosis is disrupted for LDL cholesterol.
- LDL receptors fail to internalize cholesterol efficiently.
- Consequences: plasma LDL levels rise → risk of atherosclerosis.
- Cellular effect: cholesterol-dependent pathways (membrane synthesis, steroid hormone production) are impaired.
- Demonstrates how bulk transport is critical for selective nutrient uptake.
Explain how endocytosis and exocytosis work together to remodel the plasma membrane, and describe a physiological scenario where this remodeling is critical.
- Endocytosis removes membrane sections and associated proteins from the cell surface → allows the cell to internalize receptors, transporters, or damaged membrane areas.
- Exocytosis adds new membrane components and proteins back to the plasma membrane → maintains surface area, delivers functional proteins, and repairs membrane defects.
- Dynamic balance: Continuous cycles of vesicle fusion and internalization enable the plasma membrane to adapt shape, composition, and size in response to environmental or cellular demands.
- Physiological example:
- During neurotransmission, synaptic vesicles fuse with the presynaptic membrane (exocytosis) to release neurotransmitters, then portions of the membrane are retrieved via endocytosis to recycle vesicles.
- Maintains synaptic membrane integrity while allowing rapid signaling.
