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Cell Biology - Interactive Lesson | Study Mondo
Cell Biology - Complete Interactive Lesson Part 1: Cell Structure & Organelles Cell Biology for the MCAT
Part 1 of 7 — Cell Structure & Organelles
Prokaryotes vs. Eukaryotes
Feature Prokaryotes Eukaryotes Nucleus No (nucleoid region) Yes (membrane-bound) Organelles None (membrane-bound) Many Size 1-10 μ \mu μ 10-100 μ \mu μ DNA Circular, no histones Linear, with histones Ribosomes 70S (50S + 30S) 80S (60S + 40S) Cell wall Peptidoglycan (bacteria) Cellulose (plants), chitin (fungi), none (animals)
Key Organelles
Organelle Function Key Facts Nucleus DNA storage, transcription Double membrane, nuclear pores Rough ER Protein synthesis (secretory) Ribosomes attached Smooth ER Lipid synthesis, detox No ribosomes Golgi Modify, sort, package proteins cis (receiving) → trans (shipping) Mitochondria ATP production (aerobic) Own DNA! Double membrane, maternal inheritance Lysosome Intracellular digestion pH ~5 (acidic), hydrolytic enzymes Peroxisome Oxidation, H2 _2 2
The Endomembrane System — Protein Trafficking
The MCAT frequently tests the path of a secretory protein:
Ribosome on RER → ER lumen → transport vesicle → cis-Golgi → trans-Golgi → secretory vesicle → plasma membrane \text{Ribosome on RER} \to \text{ER lumen} \to \text{transport vesicle} \to \text{cis-Golgi} \to \text{trans-Golgi} \to \text{secretory vesicle} \to \text{plasma membrane} Ribosome on RER → ER lumen → transport vesicle → cis-Golgi → trans-Golgi → secretory vesicle → plasma membrane
Signal peptide : N-terminal sequence that directs the ribosome to the RERSignal recognition particle (SRP) : Binds signal peptide and docks ribosome on RERGlycosylation begins in the ER (N-linked) and is modified in the Golgi (O-linked added)
Mannose-6-phosphate tag: targets proteins to lysosomes
Endosymbiotic Theory — Evidence Checklist
Why mitochondria (and chloroplasts) were once free-living bacteria:
Own circular DNA (like bacteria)
70S ribosomes (not 80S like the rest of the eukaryotic cell)Double membrane (inner = original bacterial membrane; outer = host's endocytic vesicle)Reproduce by binary fission
Maternal inheritance (mitochondria come from the egg)
Cytoskeleton Overview
Component Diameter Function Key Drug Microfilaments (actin) 7 nm Cell motility, muscle contraction, cleavage furrow Cytochalasin (inhibits) Intermediate filaments 10 nm Structural support (keratin, vimentin) — Microtubules (tubulin) 25 nm Mitotic spindle, cilia, flagella, intracellular transport Colchicine, taxol
Cilia : 9+2 microtubule arrangement (motile) or 9+0 (primary/sensory)Dynein : motor protein that moves cargo toward minus end (toward cell center)Kinesin : motor protein that moves cargo toward plus end (toward periphery) Cell Structure & Organelles 🎯
Passage-Style Thinking: Organelle Dysfunction
MCAT passages often describe a disease and ask you to identify the organelle involved. Key pattern recognitions:
Disease/Condition Organelle Defect Mechanism I-cell disease Golgi (M6P tagging) Lysosomal enzymes secreted instead of delivered to lysosomes Tay-Sachs Lysosome Missing hexosaminidase A → ganglioside accumulation Zellweger syndrome Peroxisome Cannot import peroxisomal enzymes → very long chain fatty acid buildup Kartagener syndrome Microtubules (dynein) Immotile cilia → situs inversus, infertility, respiratory infections
Free vs. Bound Ribosomes
Free ribosomes : Make proteins that stay in the cytoplasm (enzymes, structural proteins)Bound ribosomes (on RER): Make secretory proteins, membrane proteins, and lysosomal enzymesThe ribosome itself is identical — the signal peptide determines where it goes
This is a common MCAT distractor: the ribosome does not "know" where it needs to be in advance
Key Takeaways — Part 1
Know every organelle's function and the diseases that result from dysfunction
Protein trafficking path: RER → transport vesicle → cis-Golgi → trans-Golgi → destination
Mannose-6-phosphate = lysosome targeting signal; defects cause I-cell disease
Endosymbiotic theory evidence: circular DNA, 70S ribosomes, double membrane, binary fission
Cytoskeleton: microfilaments (actin, 7nm), intermediate filaments (10nm), microtubules (tubulin, 25nm)
Motor proteins: dynein (minus-end), kinesin (plus-end); dynein arms also drive cilia
Free ribosomes → cytoplasmic proteins; bound ribosomes → secretory/membrane/lysosomal proteins
Part 2: Membrane Transport Cell Biology for the MCAT
Part 2 of 7 — Cell Membrane & Transport
Membrane Structure (Fluid Mosaic Model)
Phospholipid bilayer : Hydrophilic heads out, hydrophobic tails inCholesterol : Regulates fluidity — prevents crystallization at low temp, prevents excess fluidity at high temp (acts as a "fluidity buffer")Integral proteins : Span the membrane (channels, receptors, transporters)Peripheral proteins : Loosely attached to surface (often via electrostatic interactions)Glycoproteins/Glycolipids : Carbohydrate chains on extracellular face only — cell recognition, immune identity
Transport Mechanisms
Type Energy? Direction Examples Simple diffusion No High → Low O2 _2 2
Part 3: Cell Signaling Cell Biology for the MCAT
Part 3 of 7 — Cell Cycle & Mitosis
The Cell Cycle
Phase Events Duration G1 _1 1 Cell growth, organelle duplication, gene expression Variable (longest) S DNA replication (each chromosome → 2 sister chromatids) ~8 hours G2 _2
Part 4: Cell Cycle & Division Cell Biology for the MCAT
Part 4 of 7 — Meiosis & Genetic Diversity
Meiosis Overview
Diploid (2n, 4C) → Meiosis I Haploid (1n, 2C) → Meiosis II 4 haploid gametes (1n, 1C) \text{Diploid (2n, 4C)} \xrightarrow{\text{Meiosis I}} \text{Haploid (1n, 2C)} \xrightarrow{\text{Meiosis II}} \text{4 haploid gametes (1n, 1C)} Diploid (2n, 4C) Meiosis I
Part 5: Apoptosis & Regulation Cell Biology for the MCAT
Part 5 of 7 — Cell Signaling
Signal Transduction — The Universal Framework
Signal (ligand) → Receptor → Transduction (amplification) → Cellular Response \text{Signal (ligand)} \to \text{Receptor} \to \text{Transduction (amplification)} \to \text{Cellular Response} Signal (ligand) → Receptor → Transduction (amplification) → Cellular Response
Signal amplification is critical: one hormone molecule can activate millions of downstream effectors through enzyme cascades. Each step multiplies the signal.
Types of Signaling
Part 6: Stem Cells & Differentiation Cell Biology for the MCAT
Part 6 of 7 — Apoptosis & Cellular Processes
Apoptosis (Programmed Cell Death)
Apoptosis is an orderly, energy-requiring process — fundamentally different from necrosis:
Cell shrinks, chromatin condenses, DNA fragments into 180 bp ladder
Membrane blebs form (but does NOT rupture — no inflammation)
"Eat me" signals (phosphatidylserine on outer leaflet) attract phagocytes
Regulated by caspases — a protease cascade
Apoptosis Pathways
Pathway Trigger Initiator Caspase Key Steps Intrinsic (mitochondrial) DNA damage, oxidative stress, growth factor withdrawal Caspase-9 Mitochondria release cytochrome c → apoptosome forms → caspase-9 activation Extrinsic (death receptor) Death ligands (FasL, TNF, TRAIL) Caspase-8 Ligand binds Fas → DISC forms → caspase-8 activation Both pathways converge → Caspase-3 (executioner)Cleaves cellular substrates → cell death
Key Regulators of Apoptosis
Part 7: Review & MCAT Practice Cell Biology for the MCAT
Part 7 of 7 — Specialized Cell Types & Tissues
The Four Tissue Types
Type Function Key Features Examples Epithelial Cover surfaces, secretion, absorption Tightly packed, avascular, basement membrane Skin, intestinal lining, glands Connective Support, connect, protect Cells in extracellular matrix (ECM) Bone, blood, cartilage, adipose, tendons Muscle Contraction and movement Contractile proteins (actin/myosin) Skeletal, smooth, cardiac Nervous Signal transmission and integration Neurons + glial cells Brain, spinal cord, peripheral nerves
Epithelial Classifications
Facilitated diffusion No High → Low Glucose (GLUT transporters), ions (channels)
Primary active transport Yes (ATP) Low → High Na+ ^+ + + ^+ + 2 + ^{2+} 2 +
Secondary active transport Yes (gradient) Low → High SGLT (Na+ ^+ + + ^+ + + ^+ +
Endocytosis Yes Into cell Phagocytosis, pinocytosis, receptor-mediated
Exocytosis Yes Out of cell Neurotransmitter release, hormone secretion
Na+ ^+ + + ^+ + Per ATP hydrolyzed: 3 Na+ ^+ + + ^+ +
Creates electrochemical gradient for both ions
Maintains resting membrane potential (~− 70 -70 − 70
Electrogenic : net positive charge moved out (3+ out vs 2+ in)Powers secondary active transport (Na+ ^+ +
Osmosis and Tonicity Solution Solute vs. Cell Water Movement Cell Response Hypotonic Less solute outside Water enters cell Swells (lysis in animal cells) Isotonic Equal solute No net movement Normal shape Hypertonic More solute outside Water leaves cell Shrinks (crenation in RBCs)
Key distinction : Osmolarity = total solute concentration. Tonicity = the effect on cell volume (only non-penetrating solutes matter). Urea is an osmole but freely crosses membranes, so it does not affect tonicity.
Membrane Selectivity: What Crosses and What Cannot
This is a fundamental MCAT reasoning skill — predicting what can cross a lipid bilayer:
Crosses freely (simple diffusion) :
Small, nonpolar molecules: O2 _2 2 2 _2 2 2 _2 2
Small, uncharged polar: H2 _2 2
Hydrophobic molecules: steroid hormones, fatty acids
Cannot cross without help :
Ions: Na+ ^+ + + ^+ + 2 + ^{2+} 2 + − ^-
Receptor-Mediated Endocytosis
Ligand binds receptor → clathrin-coated pit forms → vesicle internalized
Example: LDL cholesterol uptake via LDL receptors
Familial hypercholesterolemia : defective LDL receptors → LDL stays in blood → atherosclerosisThis is a favorite MCAT passage topic linking cell biology to disease
Membrane Potential — Nernst Equation
For a single ion, the equilibrium potential is:
E i o n = 61 z log [ i o n ] o u t s i d e [ i o n ] i n s i d e (at 37°C, in mV) E_{ion} = \frac{61}{z} \log \frac{[ion]_{outside}}{[ion]_{inside}} \text{ (at 37°C, in mV)} E i o n = z
E K ≈ − 90 E_K \approx -90 E K ≈ − 90 + ^+ + E N a ≈ + 60 E_{Na} \approx +60 Key Takeaways — Part 2
Fluid mosaic model: phospholipids + cholesterol (fluidity buffer) + integral/peripheral proteins + glycocalyx
Crossing rules: small nonpolar = free diffusion; charged/large polar = need channels or transporters
Na+ ^+ + + ^+ + + ^+ + + ^+ +
Osmolarity ≠ tonicity: only non-penetrating solutes affect cell volume (urea penetrates → does not contribute to tonicity)
Receptor-mediated endocytosis: clathrin-coated pits (LDL uptake → familial hypercholesterolemia link)
Resting membrane potential (~− - − + ^+ + + ^+ + + ^+
2
Final growth, preparation for mitosis, error checking
M Mitosis + cytokinesis ~1 hour
G0 _0 0 Quiescent state (non-dividing) Indefinite
Interphase = G1 _1 1 2 _2 2
DNA Content Through the Cell Cycle Phase Chromosomes DNA Content Chromatids G1 _1 1 2n (46) 2C 46 After S 2n (46) 4C 92 (sister chromatids joined) After mitosis 2n (46) 2C 46
Key insight : After S phase, the chromosome number does NOT double — sisters are still joined at the centromere. The DNA content doubles (2C → 4C) but chromosome count stays at 2n until anaphase of meiosis I.
Mitosis Stages (PMAT)
Prophase : Chromatin condenses → chromosomes visible. Nuclear envelope breaks down. Centrosomes migrate to poles, spindle begins forming.Prometaphase : Kinetochore microtubules attach to centromeres. Chromosomes move to center.Metaphase : Chromosomes align at metaphase plate. Spindle assembly checkpoint ensures all kinetochores are attached.Anaphase : Cohesin proteins cleaved → sister chromatids separate and are pulled to opposite poles by shortening kinetochore microtubules.Telophase : Nuclear envelopes reform around each chromosome set. Chromosomes decondense. Cytokinesis begins.
Cytokinesis
Animal cells : Cleavage furrow (contractile ring of actin and myosin pinches the cell)Plant cells : Cell plate forms from Golgi-derived vesicles (no cleavage furrow — rigid cell wall)
Cell Cycle Regulation — Cyclins and CDKs Regulatory Pair Checkpoint Function Cyclin D + CDK4/6 G1 _1 1 Respond to growth factor signals Cyclin E + CDK2 G1 _1 1 Commit to DNA replication Cyclin A + CDK2 S phase Drive replication Cyclin B + CDK1 (MPF) G2 _2 2 Trigger entry into mitosis
CDKs (cyclin-dependent kinases) are always present but inactive without their cyclin partnerCDK inhibitors (p21, p27) act as brakes — upregulated by p53
Cell Cycle Checkpoints Checkpoint Location Checks for G1 _1 1 End of G1 _1 1 DNA damage, cell size, growth signals, nutrients G2 _2 2 End of G2 _2 2 Complete DNA replication, no damage Spindle Assembly During M All chromosomes properly attached to spindle
Cancer Biology — Oncogenes vs. Tumor Suppressors
This is one of the most tested MCAT topics in cell biology. Understand the analogy:
Rb Pathway — How It Works
Rb normally binds and inhibits E2F (a transcription factor for S-phase genes)
Growth factor signals → Cyclin D/CDK4 phosphorylates Rb → releases E2F
Free E2F activates genes needed for DNA replication
If Rb is mutated: E2F is always free → uncontrolled entry into S phase
The APC/C (Anaphase-Promoting Complex)
Ubiquitin ligase activated at the metaphase-to-anaphase transition
Targets securin for degradation → separase released → cleaves cohesin → sister chromatids separate
Also targets cyclin B for degradation → MPF inactivated → cell exits mitosis
Key Takeaways — Part 3
Cell cycle: G1 _1 1 2 _2 2 1 _1 1 2 _2 2
After S phase: 46 chromosomes (unchanged), 92 chromatids, 4C DNA content
Cyclins fluctuate; CDKs are constitutive. MPF (Cyclin B + CDK1) drives M-phase entry
p53 → p21 → CDK inhibition at G1 _1 1
Oncogenes: gain-of-function, dominant (Ras, Myc, HER2). Tumor suppressors: loss-of-function, both alleles (p53, Rb, BRCA)
Rb normally sequesters E2F; phosphorylation by CDK releases E2F for S-phase gene activation
APC/C ubiquitinates securin and cyclin B → triggers anaphase and mitotic exit
Haploid (1n, 2C)
4 haploid gametes (1n, 1C)
Meiosis I vs. Meiosis II Feature Meiosis I Meiosis II Starting cells 1 diploid (2n, 4C) 2 haploid (1n, 2C) Result 2 haploid cells (1n, 2C) 4 haploid cells (1n, 1C) Homologs separate? YES (reduction division) No Sister chromatids separate? No YES Crossing over? YES (prophase I) No Unique to meiosis? YES — homologous pairing, synapsis, crossing over Similar to mitosis
Prophase I — The Key Stage Prophase I is the longest and most complex phase:
Synapsis : Homologous chromosomes pair up (form a bivalent/tetrad)Synaptonemal complex : Protein structure holds homologs togetherCrossing over : Non-sister chromatids exchange DNA segments at chiasmata This produces recombinant chromosomes with novel allele combinations
Sources of Genetic Diversity Source Mechanism Magnitude Crossing over DNA exchange between homologs in prophase I Theoretically unlimited recombination Independent assortment Random orientation of bivalents at metaphase I 2 23 ≈ 8.4 2^{23} \approx 8.4 2 23 ≈ 8.4 Random fertilization Any sperm + any egg 2 23 × 2 23 = 2 46 ≈ 70 2^{23} \times 2^{23} = 2^{46} \approx 70 2 23 × 2 23 = 2 46 ≈ 70 Random mutations Errors in replication, environmental mutagens Variable
Comparing Mitosis and Meiosis Feature Mitosis Meiosis Divisions 1 2 Daughter cells 2 (identical, 2n) 4 (unique, 1n) Crossing over No Yes (prophase I) Homolog pairing No Yes (synapsis) Purpose Growth, repair Gamete production Genetic variation None Extensive
Nondisjunction — When Chromosome Separation Fails
Error Timing Affected Gametes Result Meiosis I nondisjunction All 4 gametes are abnormal (either +1 or − - − More severe — affects ALL gametes Meiosis II nondisjunction 2 normal + 2 abnormal gametes Less severe — only 2 of 4 affected
Common aneuploidies from nondisjunction:
Trisomy 21 (Down syndrome): 3 copies of chromosome 21Turner syndrome (45, XO): only one X chromosome in femalesKlinefelter syndrome (47, XXY): extra X in malesTrisomy 18 (Edwards syndrome), Trisomy 13 (Patau syndrome)
Oogenesis vs. Spermatogenesis
Feature Spermatogenesis Oogenesis Products per meiosis 4 functional sperm 1 functional egg + 3 polar bodies Timing Continuous from puberty Begins in fetal life, arrested at prophase I until ovulation Completion ~64 days per cycle May take decades (arrested at prophase I!) Location Seminiferous tubules (testes) Ovarian follicles
Why this matters for MCAT : Older maternal age → higher nondisjunction risk because oocytes arrested in prophase I for decades, cohesin proteins degrade over time.
Ploidy vs. DNA Content — Master This Distinction
The MCAT loves to test this:
Ploidy (n) : Number of unique chromosomes (haploid = n, diploid = 2n)DNA content (C) : Amount of DNA (doubles after S phase)A cell can be 1n but 2C (after meiosis I, before meiosis II)
Always track both independently through the cell cycle
Nondisjunction & Gametogenesis 🎯
Key Takeaways — Part 4
Meiosis I: homologs separate (2n → 1n, reduction division). Meiosis II: sisters separate (like mitosis)
Prophase I is unique: synapsis, crossing over at chiasmata, recombinant chromosomes
Genetic diversity: crossing over + independent assortment (2 23 2^{23} 2 23
Nondisjunction in meiosis I → all 4 gametes abnormal; in meiosis II → 2 of 4 abnormal
Spermatogenesis → 4 functional sperm; Oogenesis → 1 egg + 3 polar bodies
Oocyte arrest at prophase I for decades → cohesin degradation → maternal age-related aneuploidy
Always track ploidy (n) and DNA content (C) independently
Endocrine Long (via blood) Slow (minutes-hours) Insulin from pancreas to muscle Paracrine Short (nearby cells) Moderate Growth factors, histamine Autocrine Self (same cell) Fast IL-2 in activated T cells Juxtacrine Direct contact Fast Notch signaling, MHC-TCR Synaptic Across synapse Very fast (ms) Neurotransmitters
Major Receptor Types Receptor Location Mechanism Ligands Example G-protein coupled (GPCR) Membrane G-protein → second messenger Water-soluble hormones, neurotransmitters Epinephrine (beta receptors) Receptor tyrosine kinase (RTK) Membrane Dimerization → autophosphorylation → Ras/MAPK Growth factors Insulin receptor, EGF receptor Ligand-gated ion channel Membrane Ion flux Neurotransmitters nAChR at NMJ Intracellular/Nuclear Cytoplasm or nucleus Direct transcription factor Lipid-soluble hormones Steroid hormones, thyroid hormone
GPCR Signaling — The Most Tested Pathway
Ligand binds GPCR (7-transmembrane domain receptor)
Conformational change → Gα \alpha α
Gα \alpha α
Gs _s s → activates adenylyl cyclase → cAMP ↑ → PKA activatedGi _i i → inhibits adenylyl cyclase → cAMP ↓Gq _q q → activates phospholipase C → IP3 _3 3
Gα \alpha α
Second Messengers Messenger Produced by Activates Key Functions cAMP Adenylyl cyclase PKA Glycogen breakdown, gene expression IP3 _3 3 Phospholipase C Ca2 + ^{2+} 2 + Smooth muscle contraction, secretion DAG Phospholipase C PKC Cell growth, differentiation Ca2 + ^{2+} 2 + Released from ER Calmodulin, many enzymes Muscle contraction, exocytosis, signaling cGMP Guanylyl cyclase PKG Vasodilation (NO pathway)
Signal Amplification — Why One Molecule Matters
MCAT passages test quantitative reasoning about amplification:
1 epinephrine → 1 GPCR → many G-proteins → many adenylyl cyclase → many cAMP → many PKA → millions of products \text{1 epinephrine} \to \text{1 GPCR} \to \text{many G-proteins} \to \text{many adenylyl cyclase} \to \text{many cAMP} \to \text{many PKA} \to \text{millions of products} 1 epinephrine → 1 GPCR → many G-proteins → many adenylyl cyclase → many cAMP → many PKA → millions of products
Each enzyme activates multiple substrates, creating an exponential amplification cascade . This is why hormones work at nanomolar concentrations.
Key Pathway Connections for MCAT
Pathway Clinical Connection Cholera toxin → Gs _s s Watery diarrhea (cAMP ↑ in intestinal cells) Pertussis toxin → Gi _i i Whooping cough (cAMP ↑ because inhibition is removed) Ras mutation (stuck ON) Cancer (30% of tumors have Ras mutations) Viagra → inhibits PDE5
Receptor Desensitization
Cells can turn down signaling when overstimulated:
Receptor phosphorylation : Kinases phosphorylate the receptor → arrestin binds → blocks G-protein couplingReceptor internalization : Endocytosis removes receptors from the surfaceDownregulation : Decreased receptor gene expressionThis explains drug tolerance and why chronic stimulation leads to diminished response
Nitric Oxide (NO) Signaling — Unique Pathway
NO is a gas that diffuses freely through membranes (no receptor needed at surface)
Activates soluble guanylyl cyclase → cGMP ↑ → PKG → smooth muscle relaxation → vasodilation
Very short-lived (seconds)
NO synthase uses arginine + O2 _2 2
Clinical: nitroglycerin releases NO → relieves angina
Key Takeaways — Part 5
Signal transduction: ligand → receptor → transduction (amplification) → response
GPCRs: Gs _s s i _i i q _q q 3 _3 3
RTKs: dimerize and autophosphorylate → Ras → MAPK cascade (growth signals)
Steroid hormones: cross membrane, bind intracellular receptors, act as transcription factors (slow but lasting)
Second messengers: cAMP, IP3 _3 3 2 + ^{2+} 2 +
Cholera = Gs _s s i _i i
Signal amplification: each cascade step multiplies the signal exponentially
NO: gaseous signal → guanylyl cyclase → cGMP → vasodilation
Bcl-2 Anti-apoptotic (blocks cytochrome c release) Overexpressed in follicular lymphoma Bax, Bak Pro-apoptotic (form pores in mitochondria → cytochrome c release) Promote apoptosis p53 Pro-apoptotic (upregulates Bax, activates intrinsic pathway) Mutated in >50% of cancers IAPs Inhibitors of apoptosis (bind and inhibit caspases) Can contribute to cancer survival Smac/DIABLO Inhibits IAPs → promotes apoptosis Released from mitochondria with cytochrome c
Apoptosis vs. Necrosis Feature Apoptosis Necrosis Trigger Internal signals, death receptors Trauma, toxins, ischemia Process Orderly, controlled shrinkage Chaotic cell swelling and lysis Membrane Intact (blebs but no rupture) Ruptures → contents leak out Inflammation No Yes (leaking contents trigger immune response)Energy (ATP) Required Not required DNA Fragmented in ~180 bp ladders (nucleosomal) Random degradation/smear
Autophagy — Self-Eating for Survival
Autophagy is distinct from apoptosis — it is a survival mechanism , not a death pathway:
Cell digests its own damaged organelles or misfolded proteins
Double-membrane vesicle (autophagosome) engulfs target → fuses with lysosome → contents degraded
Activated by nutrient deprivation, stress, mTOR inhibition
Provides amino acids and energy during starvation
MCAT distinction : Apoptosis = programmed cell DEATH. Autophagy = programmed cell SURVIVAL under stress.
Necroptosis — Programmed Necrosis
A regulated form of necrosis (combines features of both)
Triggered by death receptors (like extrinsic apoptosis) but when caspase-8 is inhibited
RIPK1 → RIPK3 → MLKL → membrane rupture
Results in inflammation (like necrosis) but is genetically programmed (like apoptosis)
Clinical Connections — MCAT Favorites
Condition Apoptosis Connection Cancer Too little apoptosis (Bcl-2 overexpression, p53 loss) Autoimmune disease Too little apoptosis of self-reactive lymphocytes Alzheimer's, Parkinson's Excessive neuronal apoptosis HIV/AIDS Excessive CD4+ T cell apoptosis Development Apoptosis removes webbing between fingers, shapes organs
During Development — Apoptosis Is Essential
Removes cells between developing fingers and toes
Eliminates self-reactive T cells in the thymus (negative selection)
Shapes the nervous system by removing neurons without proper connections
The tadpole tail resorbs during metamorphosis via apoptosis
Key Takeaways — Part 6
Apoptosis: orderly, ATP-requiring, no inflammation. Necrosis: chaotic, membrane rupture, inflammation.
Intrinsic: stress → Bax/Bak pores → cytochrome c released → caspase-9. Extrinsic: death ligand → caspase-8. Both → caspase-3.
Bcl-2 = anti-apoptotic (cancer when overexpressed); p53 and Bax = pro-apoptotic
DNA ladder (~180 bp) = apoptosis. DNA smear = necrosis.
PS exposure on outer membrane = "eat me" signal for phagocytes
Autophagy = survival mechanism (self-digestion under stress), NOT death
Apoptosis essential in development (digit separation, thymic negative selection, neural pruning)
Too little apoptosis → cancer; too much → neurodegeneration, immunodeficiency
Squamous (flat) Simple Simple squamous Alveoli, capillaries, Bowman's capsule Squamous Stratified Stratified squamous Skin, esophagus, vagina (protection) Cuboidal Simple Simple cuboidal Kidney tubules, thyroid follicles Columnar Simple Simple columnar Intestinal lining (with goblet cells) Columnar Pseudostratified Pseudostratified columnar Trachea (ciliated, with goblet cells) Various Multiple layers Transitional Bladder (stretches)
Rule : Simple = one layer (diffusion/absorption). Stratified = multiple layers (protection).
Muscle Types — Comparison Feature Skeletal Cardiac Smooth Striated? Yes Yes No Voluntary? Yes No (autonomic) No (autonomic) Nuclei Multinucleated (peripheral) 1-2 central nuclei 1 central nucleus Special features T-tubules, sarcoplasmic reticulum Intercalated discs (gap junctions + desmosomes) Gap junctions, no sarcomeres Repair capacity Limited (satellite cells) Very limited Good (can proliferate) Contraction speed Fast Intermediate Slow, sustained
Connective Tissue Components
Collagen : Most abundant protein in the body; provides tensile strength (Type I in bone/tendon, Type II in cartilage, Type IV in basement membranes)Elastin : Allows stretch and recoil (lungs, arteries, skin)Fibroblasts : Produce collagen and ECM componentsGround substance : Gel-like matrix of proteoglycans and glycosaminoglycans (GAGs) Stem Cells — Potency Hierarchy
Type Potency Can Become Example Totipotent Everything Any cell type + extraembryonic tissue (placenta) Zygote, early morula Pluripotent Almost everything Any of the 3 germ layers but NOT placenta Embryonic stem cells (inner cell mass) Multipotent Several related types Cells within one lineage Hematopoietic stem cells → all blood cells Oligopotent Few types Limited cell types Lymphoid progenitor → T, B, NK cells Unipotent One type Only one differentiated cell type Satellite cells → skeletal muscle only
Cell Junctions — Holding Tissues Together
Junction Function Key Proteins Found In Tight junctions (zonula occludens) Seal between cells (barrier) Claudins, occludins Intestinal epithelium, BBB Adherens junctions Cell-cell adhesion Cadherins (Ca2 + ^{2+} 2 + Epithelial tissues Desmosomes Strong mechanical attachment Cadherins (desmogleins) + intermediate filaments Skin, cardiac muscle Gap junctions Direct cell-cell communication Connexins → connexons Cardiac muscle, smooth muscle Hemidesmosomes Cell-to-basement membrane Integrins + intermediate filaments Epithelial base
Extracellular Matrix (ECM) Signaling
Integrins : Transmembrane receptors linking ECM to cytoskeletonBidirectional signaling: "outside-in" (ECM signals affect cell behavior) and "inside-out" (cell regulates integrin adhesion)
ECM composition influences cell fate: stiff ECM → bone differentiation; soft ECM → neuronal differentiation
Matrix metalloproteinases (MMPs) : Enzymes that degrade ECM (important in wound healing, but exploited by cancer cells for invasion/metastasis)
Germ Layer Origins — What Comes From Where
Germ Layer Derivatives Ectoderm Nervous system, skin epidermis, hair, nails, lens, enamel Mesoderm Muscle, bone, blood, heart, kidneys, gonads, connective tissue Endoderm GI tract lining, liver, pancreas, lung lining, thyroid, bladder
Cell Biology — Complete! ✅
Key Takeaways — Part 7
Four tissue types: epithelial (cover), connective (support), muscle (contract), nervous (signal)
Epithelial: simple = 1 layer (exchange); stratified = multiple layers (protection). Shape: squamous, cuboidal, columnar
Muscle: skeletal (voluntary, striated), cardiac (involuntary, striated, intercalated discs), smooth (involuntary, non-striated)
Collagen: most abundant protein; vitamin C required for hydroxylation (scurvy connection)
Stem cell potency: totipotent → pluripotent → multipotent → oligopotent → unipotent
Cell junctions: tight (barrier), adherens/desmosomes (adhesion), gap (communication), hemidesmosomes (to basement membrane)
Integrins: link ECM to cytoskeleton; bidirectional signaling
Germ layers: ectoderm (nerves, skin), mesoderm (muscle, bone, blood), endoderm (GI lining, liver, lungs)
−
Large polar molecules: glucose, amino acids
Macromolecules: proteins, nucleic acids
61
log
[ i o n ] in s i d e [ i o n ] o u t s i d e
(at 37°C, in mV)
E N a
≈
+ 60
Resting potential (~− 70 -70 − 70 E K E_K E K + ^+ + +
Prevents cGMP breakdown → vasodilation
Caffeine → inhibits phosphodiesterase cAMP stays elevated → sympathetic-like effects