#plasma membrane

Basics of Cell Biology

Which of the following is true about the Fluid Mosaic Model?

Fluid Mosaic Model postulated by Singer and Nicolson in 1972 integrated thermodynamic considerations and experimental data that membranes behave as two-dimensional fluid solutions. Phospholipids and sphingolipids undergo rapid lateral diffusion measured 1-3 µm2/s, rotation around axis, transbilayer flip-flop rare without flippase catalysis, demonstrated by Frye and Edidin fusion of human and mouse fibroblasts where surface antigens intermix within 40 minutes, and later single-particle tracking revealing Brownian, confined, and directed motions due to cytoskeletal fences. Integral membrane proteins float in lipid sea, some tethered via ankyrin to spectrin cortex, others partitioning into cholesterol-rich ordered rafts enriched in sphingomyelin for signaling. Peripheral proteins attach via ionic interactions or lipid anchors myristoylation, palmitoylation. Lipid asymmetry is maintained by ATP-dependent P4-ATPases. Membrane is not static nor rigid, lipids and proteins can move laterally, asymmetry persists except during apoptosis, enabling processes like immune synapse, vesicular budding, and hormone reception that require reorganization of components in plane of membrane.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 10: Fluid Mosaic Model, Lateral Diffusion.

View Details

Basics of Cell Biology

Which component of the plasma membrane is responsible for fluidity?

Membrane fluidity describes lateral mobility, rotation, and flexing of components, parameter influencing permeability, fusion, and signaling complex formation. Phospholipids primarily determine fluidity through acyl chain composition: presence of cis double bonds as in oleoyl 18:1 and arachidonoyl 20:4 introduces kinks preventing close packing, lowering melting temperature Tm and increasing lateral diffusion coefficient about 10^-8 cm2/s measured by fluorescence recovery after photobleaching and fluorescence anisotropy. Shorter chains also increase fluidity. Cholesterol buffers fluidity by intercalating with rigid ring near chains, reducing motion at high temperature while preventing crystallization at low temperature, broadening phase transition. Proteins and carbohydrates can locally restrict diffusion via cytoskeletal corrals and lectin crosslinking, but bulk fluidity originates from lipids. Ribosomes associated with rough ER translation do not influence plasma membrane lipid order. Regulated desaturase enzymes SCD1 introducing double bonds adjust fluidity in response to cold, diet, and insulin signaling, essential for maintaining receptor tyrosine kinase activity and cold tolerance in poikilotherms.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Phospholipids and Fluidity Regulation.

View Details

Basics of Cell Biology

Which scientist proposed the Unit Membrane Model?

Early electron microscopy after osmium fixation revealed trilaminar image of membranes about 7.5 nm thick: two dark lines 2 nm each representing protein stained by osmium, light core of lipid. J. David Robertson at Harvard analyzed myelin, chloroplast, and plasma membranes and in 1959 proposed Unit Membrane Model asserting all biological membranes share same basic construction of lipid bilayer sandwiched between non-lipid layers, with asymmetry that inner and outer surfaces differ chemically, explaining functional polarity. Robertson emphasized continuity of membranes through ER and nuclear envelope and suggested proteins extended as sheets. This unified view improved over Davson-Danielli paucimolecular sandwich which proposed protein layers without EM proof, and provided terminology unit membrane widely used in histology. Although later Singer and Nicolson showed proteins are globular amphipathic entities embedded within fluid lipid phase rather than extended coats, Robertson's model was pivotal for recognizing universal bilayer organization and inspiring later fluid mosaic concept, placing bilayer as central architectural principle.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Unit Membrane Model, Robertson.

View Details

Basics of Cell Biology

Which model of the plasma membrane first introduced the idea of a lipid bilayer?

Early membrane theories debated whether lipid or protein formed continuous barrier. Charles Overton's permeability studies correlated anesthetic potency with oil solubility hinting at lipid membrane, but direct bilayer demonstration came from Evert Gorter and François Grendel at Leiden in 1925. They extracted erythrocyte lipids with acetone, spread them as monolayer at Langmuir trough air-water interface, and measured area at collapse pressure. Total lipid area approximated double surface area of red cells used, leading to inference that membrane consists of two opposed lipid layers with non-polar tails inward, polar heads outward. Despite experimental limitations underestimating lipid amount and ignoring protein contribution, conceptual breakthrough established lipid bilayer as core structure. Subsequent refinements included Davson-Danielli sandwich model proposing protein layers coating bilayer based on surface tension, Robertson's unit membrane EM trilaminar interpretation, and finally Singer-Nicolson fluid mosaic incorporating proteins within fluid lipid sea. Thus Gorter-Grendel experiment stands as first bilayer proposal foundational for modern membrane biology.

Ref: Lodish et al., Molecular Cell Biology, 9th ed., Chapter 7: Gorter and Grendel Bilayer Experiment.

View Details

Basics of Cell Biology

Which of the following is not a function of the plasma membrane?

Plasma membrane confers cell individuality by separating intracellular milieu from external environment and actively regulating exchange to maintain homeostasis. Its phospholipid bilayer plus embedded transport machinery including Na+/K+ ATPase establishing 140 mM potassium inside and 145 mM sodium outside, glucose carriers GLUT family facilitating uptake, amino acid exchangers, and aquaporins ensuring selective permeability and volume control, together with tight junctions restricting paracellular diffusion. Signaling platforms include receptor tyrosine kinases like EGFR that dimerize upon EGF binding activating Ras-MAPK and PI3K-Akt cascades, heterotrimeric GPCRs coupling to adenylyl cyclase producing cAMP activating PKA, and integrins linking extracellular matrix fibronectin and laminin to actin cytoskeleton for mechanotransduction via focal adhesion kinase. Glycoproteins and glycolipids presenting sialylated and fucosylated epitopes mediate cell-cell recognition essential for immune surveillance, tissue patterning, and blood grouping. Protein synthesis occurs elsewhere: cytosolic free 80S ribosomes translate cytosolic proteins, ER-bound ribosomes synthesize secretory proteins translocated via Sec61 channel, with mRNA processing in nucleus. Therefore synthesis of proteins is not intrinsic plasma membrane function.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Plasma Membrane Functions Overview.

View Details

Plasma Membrane

Which of the following is NOT a feature of plasma membrane lipids?

Plasma membrane lipids assemble through non-covalent forces rather than covalent polymerization. Each phospholipid or cholesterol monomer inserts via hydrophobic effect with tails buried together while polar headgroups contact water, stabilized by van der Waals contacts, hydrogen bonding between phosphate oxygens and water, and electrostatic interactions. This allows lateral diffusion, rotation, and exchange between leaflets catalyzed by flippases, and reversible desorption to cytosolic carriers. Membranes exhibit selective permeability because polar headgroup region impedes hydrophobic solutes while hydrocarbon core impedes polar solutes, requiring transporters. They self-assemble into bilayers spontaneously when amphipathic lipids reach critical micelle concentration, forming vesicles that encapsulate aqueous contents, principle exploited for liposomal drug delivery. If lipids were covalently bonded together like polymers, fluidity would be lost, proteins could not diffuse, and processes like cell fusion, cytokinesis, and endocytosis would be impossible. Consequently fluidity, repair, and remodeling depend on non-covalent nature, with proteins providing scaffold but not crosslinking lipids permanently.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Non-Covalent Assembly of Lipids.

View Details

Plasma Membrane

Which type of lipid is NOT a part of the plasma membrane?

Biological membrane formation is governed by amphipathic geometry where polar headgroup cross-section balances hydrophobic tail volume, satisfying packing parameter close to 1 for bilayer assembly and stability. Phospholipids such as phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, sphingolipids like sphingomyelin and cerebroside, and cholesterol as small amphiphile intercalated among chains all meet this criterion and readily incorporate into 5 nanometer fluid mosaic film with integral proteins diffusing laterally. Triglycerides, triacylglycerols composed of glycerol esterified to three fatty acids lacking phosphate, sugar, or charged moiety, are completely apolar with no amphipathic character, unable to orient with one end in water. In aqueous environment they coalesce into bulk oil phase, phase separating rather than forming lamellae. Cells store triglycerides in lipid droplet organelles comprising neutral hydrophobic core surrounded by phospholipid monolayer decorated with perilipins and seipin, located in cytosol or within ER lumen for VLDL assembly in liver. Adipocytes contain large droplets for energy reserve mobilized by hormone-sensitive lipase and lipolysis. Therefore plasma membrane excludes triglycerides, which would compromise barrier integrity and fluidity.

Ref: Lehninger Principles of Biochemistry, 8th ed., Chapter 10: Triglycerides vs Membrane Lipids.

View Details

Plasma Membrane

Which of the following phospholipids is most abundant in the outer leaflet of the plasma membrane?

Quantitative lipidomics using phospholipase treatment, chemical labeling, and mass spectrometry shows outer leaflet of mammalian plasma membrane is dominated by choline-containing lipids: phosphatidylcholine roughly 60% of outer phospholipid and sphingomyelin nearly exclusively outer, together creating relatively neutral, saturated, raft-competent surface that interacts with extracellular environment and immune system. Their cylindrical shape stabilizes flat outer leaflet and protects from opsonization by complement. In contrast phosphatidylserine and phosphatidylethanolamine concentrate 75 to 90% in inner leaflet facing cytosol where their anionic and conical properties facilitate generation of negative curvature for endocytosis, binding of polycationic domains of Ras and annexins including annexin A2, and support for protein kinase C activation. Phosphatidylinositol and its phosphorylated derivatives also inner, providing platform for cytoskeleton attachment via ERM proteins and clathrin adaptors. Cardiolipin with four acyl chains is signature of inner mitochondrial membrane where it binds respiratory complexes, absent from plasma membrane. Therefore phosphatidylcholine outer enrichment reflects active sorting by P4-ATPases and thermodynamic preference, essential for charge asymmetry and signaling integrity.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Outer Leaflet Enrichment of PC.

View Details

Plasma Membrane

Which of the following is NOT a function of cholesterol in the plasma membrane?

Cholesterol's structure with rigid tetracyclic ring system and short iso-octyl tail allows it to insert into phospholipid bilayers with hydroxyl near phospholipid carbonyls and ring system interacting with upper acyl chains. At low temperatures it disrupts tight packing of saturated chains, preventing transition to gel phase and preserving lateral diffusion essential for protein function, while at high temperatures its rigid ring restricts chain motion, decreasing permeability to small polar molecules, protons, and sodium ions, maintaining electrochemical gradients. Within membranes cholesterol drives formation of liquid-ordered lipid rafts that concentrate GPI-anchored proteins and Src kinases for signaling. Beyond barrier modulation, cholesterol is substrate for mitochondrial P450scc that cleaves side chain to pregnenolone, precursor for glucocorticoids, mineralocorticoids, sex steroids, bile acids, and vitamin D. Passive transport of glucose through GLUTs or water through aquaporins does not require cholesterol as facilitator; proteinaceous pores and carriers mediate downhill movement independent of sterol content, so cholesterol does not act as transport facilitator.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Cholesterol Functions and Steroidogenesis.

View Details

Plasma Membrane

What is the primary function of glycolipids in the plasma membrane?

Glycolipids are restricted to the exoplasmic leaflet where their oligosaccharide chains, assembled in Golgi by glycosyltransferases and glycosidases, face extracellular milieu forming glycocalyx extending beyond protein domains. This topology makes them poorly suited to regulate fluidity, which is governed by fatty acid saturation and cholesterol content, or to transport ions, mediated by channels and pumps. Their principal contribution lies in recognition and signaling. Carbohydrate moieties constitute ABO and Lewis blood group antigens, selectin ligands like sialyl Lewis X that direct leukocyte rolling and extravasation, and specific receptors for microbes: GM1 ganglioside binds cholera toxin B subunit, Gb3 binds Shiga toxin, and sulfatide binds influenza virus. Clustering in cholesterol-rich lipid rafts amplifies avidity through multivalent carbohydrate-lectin interactions, organizing signal transduction and sorting in polarized epithelia. In nervous system, gangliosides modulate Trk receptor activity and neurite outgrowth. Thus glycolipid function exemplifies how membrane lipid chemical diversity translates into identity cues guiding development, immunity, and pathogen interactions rather than bulk membrane mechanics.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Glycocalyx and Cell Recognition.

View Details

Plasma Membrane

Which of the following is a major glycolipid found in the plasma membrane?

Gangliosides are prominent glycosphingolipids of vertebrate plasma membranes, characterized by a hydrophobic ceramide anchor embedded in the outer leaflet linked to a complex oligosaccharide carrying one or more sialic acid residues. This bulky carbohydrate headgroup projects into the extracellular space and participates in the glycocalyx, mediating cell-cell recognition, modulation of receptor tyrosine kinases such as EGFR, and adhesion during neural development and immune synapse formation. Unlike sphingomyelin which incorporates phosphocholine as headgroup via phosphodiester bond, or phosphatidylinositol which is a glycerophospholipid with inositol phosphate, gangliosides are synthesized stepwise in the Golgi apparatus by glycosyltransferases that sequentially add galactose, N-acetylgalactosamine, and sialic acid to ceramide arriving from ER on CERT transporter. Their saturated chains favor association with cholesterol in lipid rafts, increasing local concentration. Functionally they serve as antigenic determinants, regulators in neurogenesis, and docking sites for bacterial toxins like cholera and tetanus, illustrating how carbohydrate diversity confers recognition specificity beyond simple barrier function in physiology.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 10: Membrane Structure, Glycosphingolipids and Gangliosides.

View Details

Plasma Membrane

Which of the following stabilizes the plasma membrane by modulating its fluidity?

Modulation membrane order cholesterol textbook example fluidity homeostasis buffering mechanism dual action concentration dependent. Cholesterol inserts three beta hydroxyl near phospholipid ester carbonyl forming hydrogen bond rigid tetracycle parallel upper ten carbons acyl chains restricting trans gauche isomerization high temperatures decreasing lateral diffusion coefficient from one to zero point five micrometer squared per second and passive permeability small solutes two to three fold measured calcein leakage assays. Low temperatures cholesterol disrupts all trans crystalline lattice introducing kinks increasing free volume preventing gel phase quantified decrease order parameter S zero point eight to zero point five ESR spin label DPH anisotropy experiments broadening DSC transition. Net effect broadened phase transition abolishing sharp DSC peak buffering fluidity optimal Na K ATPase receptor function signaling. Glycoproteins mediate adhesion migration immunity, phosphatidylinositol transiently phosphorylated signaling but bulk fluidity regulated sterol, integral proteins immobilize annular lipids via picket fence but not buffer globally. Understanding cholesterol stabilization explains raft liquid ordered existence adaptation temperature dietary changes statin therapy impacts membrane order atherosclerosis pathology relevant physiology pharmacology questions exams and membrane protein function regulation.

Ref: Krause & Regen, JACS 2005, Cholesterol regulates fluidity stability buffering phase transition mechanism.

View Details