CLEP Biology Quick Review

Water's polarity and hydrogen bonding underlie nearly every biochemical property tested, and the four macromolecule classes are built and broken by the same two reverse reactions.

Water: cohesion, adhesion, high specific heat, universal solvent, less dense as ice. Carbohydrates: monosaccharides (glucose, $C_6H_12O_6$) $arrow$ disaccharides $arrow$ polysaccharides (starch, glycogen, cellulose) via glycosidic bonds. Lipids: nonpolar; triglycerides = glycerol + 3 fatty acids; phospholipids form bilayers. Proteins: 20 amino acids linked by peptide bonds; primary through quaternary structure. Nucleic acids: nucleotide = sugar + phosphate + base; DNA vs.\ RNA differ in sugar (deoxyribose vs.\ ribose) and bases (thymine vs.\ uracil).

Dehydration synthesis (releases $H_2O$, builds polymers) vs.\ hydrolysis (adds $H_2O$, breaks polymers) --- the exam often flips which direction requires water input vs.\ output.

Assuming lipids are structurally unimportant; forgetting phospholipids' amphipathic nature (hydrophilic head/hydrophobic tail) is exactly what drives spontaneous membrane bilayer formation.

Polymers build by dehydration ($-H_2O$) $arrow$ break by hydrolysis ($+H_2O$).

Chemical evolution models propose that simple organic monomers formed abiotically before self-replicating, catalytic molecules gave rise to the first cells.

Miller-Urey experiment (1953) simulated the early atmosphere (CH$_4$, NH$_3$, H$_2$, H$_2$O) with an electric spark, producing amino acids --- support for abiotic synthesis of organic monomers. RNA World hypothesis: RNA served as both a self-replicating molecule and a catalyst (ribozyme) before DNA and proteins took over those roles.

Miller-Urey (abiotic synthesis of monomers) vs.\ the RNA World hypothesis (self-replication and catalysis) --- these describe different stages of chemical evolution.

Confusing disproven ``spontaneous generation'' (complex organisms arising instantly from non-living matter, refuted by Pasteur) with modern abiogenesis (gradual chemical evolution of simple organic molecules) --- the CLEP treats these as conceptually distinct claims.

Miller-Urey $arrow$ monomers; RNA World $arrow$ self-replication.

Each organelle's structure directly enables a specific function within the eukaryotic division of labor.

Nucleus (DNA storage/transcription); mitochondria (ATP via aerobic respiration, own DNA); chloroplast (photosynthesis, own DNA); rough ER (protein synthesis/processing, ribosome-studded); smooth ER (lipid synthesis, detoxification); Golgi apparatus (modifies, packages, ships proteins); lysosomes (hydrolytic digestion); ribosomes (protein synthesis, free or bound); cytoskeleton (microtubules, microfilaments, intermediate filaments --- shape and movement).

Rough ER (ribosome-studded, makes proteins destined for secretion or membranes) vs.\ smooth ER (no ribosomes; lipid synthesis and detoxification).

Assuming mitochondria and chloroplasts occur in all eukaryotic cells --- chloroplasts are restricted to plants/algae, and both organelles are semi-autonomous with their own circular DNA (endosymbiotic origin), dividing independently of the cell cycle.

Mitochondria = powerhouse (respiration); chloroplast = solar panel (photosynthesis); both endosymbiotic.

The fluid mosaic model explains why the membrane is selectively permeable: a phospholipid bilayer studded with proteins controls exactly what crosses.

Passive transport: diffusion, facilitated diffusion (channel/carrier proteins, no ATP), osmosis (water movement, high to low water potential). Active transport requires ATP and moves solutes against their gradient (e.g., Na$^+$/K$^+$ pump). Endocytosis/exocytosis handle bulk transport. Tonicity: hypotonic (cell swells/lyses), hypertonic (cell shrinks/crenates), isotonic (no net change).

Diffusion (passive, no protein needed) vs.\ facilitated diffusion (passive, but requires a channel or carrier protein) --- both are passive and are easily mistaken for active transport.

Labeling a plant cell in a hypotonic solution as ``bursting'' --- the rigid cell wall prevents lysis; the cell instead becomes turgid.

Hypertonic = shrink; hypotonic = swell (animal) / turgid (plant); isotonic = no change.

Prokaryotes lack a true nucleus and membrane-bound organelles; eukaryotes compartmentalize their functions.

Prokaryotes (bacteria, archaea): no nucleus, circular DNA in a nucleoid, 70S ribosomes, cell wall, reproduce by binary fission, smaller (1--10 $$m). Eukaryotes: membrane-bound nucleus and organelles, linear DNA with histones, 80S ribosomes, larger (10--100 $$m), reproduce by mitosis/meiosis.

Bacterial cell wall (peptidoglycan) vs.\ plant cell wall (cellulose) vs.\ fungal cell wall (chitin) --- three different structural molecules commonly swapped on the exam.

Treating archaea as bacteria --- archaea form a distinct domain with unique membrane lipids and cell-wall chemistry (no peptidoglycan) despite a superficially prokaryotic body plan.

Pro = no nucleus, 70S ribosomes; Eu = nucleus + organelles, 80S ribosomes.

Enzymes are protein catalysts that lower activation energy by stabilizing the transition state, without being consumed in the reaction.

Substrate binds the active site (induced-fit model). Cofactors = inorganic ions (Mg$^2+$, Zn$^2+$); coenzymes = organic helpers (NAD$^+$, FAD, vitamins). Activity depends on temperature, pH, and substrate concentration, each with an optimum. Inhibition: competitive (binds the active site; outcompeted by more substrate) vs.\ noncompetitive/allosteric (binds elsewhere, changes shape; not overcome by substrate). Feedback inhibition regulates metabolic pathways.

Competitive inhibition (rate restored by adding more substrate) vs.\ noncompetitive inhibition (rate NOT restored by more substrate, because the inhibitor distorts the enzyme's shape at an allosteric site).

Assuming higher temperature always speeds up enzyme activity --- beyond the optimum, heat denatures the enzyme (disrupts tertiary structure) and activity collapses.

Competitive $arrow$ beat it with substrate; noncompetitive $arrow$ shape is broken, substrate can't help.

Cellular respiration oxidizes glucose in stages to capture energy as ATP, with oxygen as the final electron acceptor in the aerobic pathway.

Overall: $C_6H_12O_6 + 6O_2 arrow 6CO_2 + 6H_2O + ATP ( 36--38)$. Glycolysis (cytoplasm): glucose $arrow$ 2 pyruvate, net 2 ATP, 2 NADH, does not require oxygen. Pyruvate oxidation and the Krebs (citric acid) cycle (mitochondrial matrix): produces NADH, FADH$_2$, and CO$_2$. Electron transport chain and chemiosmosis (inner mitochondrial membrane): NADH/FADH$_2$ donate electrons, O$_2$ accepts them forming H$_2$O, driving ATP synthase for the bulk of ATP yield. Fermentation regenerates NAD$^+$ anaerobically (lactic acid in animals; ethanol + CO$_2$ in yeast) without extra net ATP beyond glycolysis.

Substrate-level phosphorylation (direct enzymatic transfer of a phosphate to ADP, in glycolysis and the Krebs cycle) vs.\ oxidative phosphorylation (ATP synthase powered by the proton gradient from the ETC, source of most ATP).

Forgetting glycolysis occurs in the cytoplasm and does not require oxygen --- students wrongly place all of respiration inside the mitochondria.

Glycolysis (cytoplasm) $arrow$ Krebs (matrix) $arrow$ ETC (inner membrane) $arrow$ big ATP payoff.

Photosynthesis converts light energy into chemical energy: the light reactions generate ATP and NADPH, and the Calvin cycle uses them to fix carbon into sugar.

Overall: $6CO_2 + 6H_2O + light arrow C_6H_12O_6 + 6O_2$. Light reactions (thylakoid membrane): chlorophyll absorbs light; Photosystem II splits water (photolysis, releasing O$_2$) and feeds electrons through an electron transport chain to Photosystem I, generating ATP (chemiosmosis) and NADPH. Calvin cycle (stroma): uses ATP/NADPH to fix CO$_2$ via RuBisCO into G3P, regenerating RuBP.

Photosystem II (splits water, releases O$_2$, passes electrons ``downhill'' first) vs.\ Photosystem I (re-energizes electrons, passes them to NADP$^+$ to form NADPH) --- PS II acts before PS I despite the numbering.

Calling the Calvin cycle ``light-independent'' and assuming it runs indefinitely in the dark --- it depends on the ATP/NADPH supplied by the light reactions and stops once those run out.

Light reactions: $H_2O arrow O_2$, make ATP/NADPH; Calvin cycle: $CO_2 arrow$ glucose using ATP/NADPH.

Mitosis produces two genetically identical diploid daughter cells for growth and repair through one round of nuclear division.

Cell cycle: Interphase (G1, S --- DNA replication, G2) $arrow$ Mitosis: Prophase (chromosomes condense, spindle forms), Metaphase (chromosomes align at the metaphase plate), Anaphase (sister chromatids separate to opposite poles), Telophase (nuclear envelopes reform) $arrow$ Cytokinesis (cleavage furrow in animals; cell plate in plants). Checkpoints (G1, G2, M) and cyclin/CDK complexes regulate progression.

Chromosome vs.\ chromatid --- a replicated chromosome consists of two sister chromatids joined at the centromere; chromosome NUMBER doesn't double until anaphase separates the chromatids.

Miscounting chromosome number after S phase --- DNA content doubles, but chromosome number stays the same until sister chromatids separate in anaphase.

PMAT: Prophase, Metaphase, Anaphase, Telophase $arrow$ identical diploid cells.

Meiosis halves chromosome number and shuffles genetic material across two divisions to produce genetically unique haploid gametes.

Meiosis I (reductional): homologous chromosomes separate; crossing over in prophase I creates recombination; independent assortment of homolog pairs. Meiosis II (equational): sister chromatids separate, mechanically like mitosis. Result: four non-identical haploid cells. Sources of variation: crossing over, independent assortment, random fertilization.

Meiosis I (homologs separate, reduces chromosome number, unique to meiosis) vs.\ Meiosis II (sister chromatids separate, resembles mitosis).

Placing crossing over in prophase II instead of prophase I --- recombination occurs during prophase I, a frequently mislocated event.

Meiosis I separates homologs (reduction); Meiosis II separates chromatids (like mitosis).

DNA's double helix and complementary base pairing enable faithful, semiconservative replication.

Watson-Crick model: antiparallel double helix, sugar-phosphate backbone, bases pair A-T (2 H-bonds) and G-C (3 H-bonds). Replication is semiconservative: DNA polymerase synthesizes the new strand 5$'$$arrow$3$'$ and requires a primer; the leading strand is continuous, the lagging strand discontinuous (Okazaki fragments joined by ligase); helicase unwinds the helix, topoisomerase relieves supercoiling.

Semiconservative replication (each new molecule = 1 old strand + 1 new strand, confirmed by the Meselson-Stahl experiment) vs.\ the disproven conservative and dispersive models.

Assuming DNA polymerase can synthesize 3$'$$arrow$5$'$ --- it only adds nucleotides 5$'$$arrow$3$'$, which is exactly why the lagging strand must be built discontinuously.

A-T (2 bonds), G-C (3 bonds); replication is semiconservative, synthesis always 5$'$$arrow$3$'$.

The central dogma (DNA $arrow$ RNA $arrow$ protein) describes how genetic information is decoded into functional proteins.

Transcription (nucleus): RNA polymerase synthesizes mRNA from a DNA template; pre-mRNA is processed (5$'$ cap, poly-A tail, splicing removes introns and keeps exons). Translation (ribosome): mRNA codons (triplet code, 64 codons, redundant; start = AUG; stops = UAA/UAG/UGA) are read by tRNA anticodons carrying amino acids; ribosome sites A (aminoacyl), P (peptidyl), E (exit); the polypeptide elongates until a stop codon is reached.

Transcription (DNA $arrow$ RNA, nucleus) vs.\ translation (RNA $arrow$ protein, ribosome/cytoplasm) --- students often reverse which molecule is template vs.\ product.

Forgetting RNA uses uracil (U) instead of thymine (T) when pairing with the DNA template's adenine --- a base-substitution slip.

DNA $arrow$(transcription)$arrow$ mRNA $arrow$(translation)$arrow$ protein.

Mutations alter DNA sequence with effects ranging from silent to catastrophic, and gene regulation determines which genes are actually expressed.

Point mutations: silent (no amino-acid change, degenerate code), missense (different amino acid), nonsense (premature stop codon). Frameshift mutations: insertions/deletions not in multiples of 3 shift the entire downstream reading frame. Gene regulation: prokaryotic operons (e.g., the inducible lac operon --- repressor, operator, promoter); regulatory vs.\ structural genes; eukaryotic transcription factors, enhancers, and epigenetic modification (methylation).

Missense mutation (one amino acid changes; protein may still function) vs.\ nonsense mutation (premature stop codon; usually destroys protein function).

Treating every frameshift mutation as equally severe regardless of position --- a frameshift near the very end of a gene affects less of the downstream protein than one near the start.

Silent = no change; missense = 1 aa swap; nonsense = early stop; frameshift = insertion/deletion shifts everything.

Viruses are non-cellular obligate intracellular parasites that hijack host machinery; classic transformation experiments established DNA as the genetic material.

Viruses: protein capsid plus a DNA or RNA core, some enveloped. Lytic cycle: immediate replication and host cell lysis. Lysogenic cycle: viral DNA integrates as a prophage and replicates with the host until induced into the lytic cycle. Griffith's transformation experiment (1928) showed a heritable ``transforming principle'' could convert harmless bacteria into virulent bacteria; Avery, MacLeod, and McCarty (1944) identified DNA as that principle; the Hershey-Chase bacteriophage experiment (1952) confirmed DNA (not protein) is the genetic material.

Lytic cycle (virus immediately replicates and destroys the host cell) vs.\ lysogenic cycle (viral genome integrates and lies dormant as a prophage before eventual induction).

Forgetting viruses are not classified as independently living organisms --- they lack their own metabolism and cannot reproduce outside a host cell.

Lytic = kill now; lysogenic = hide, then kill later. Griffith $arrow$ transformation; Avery et al.\ $arrow$ DNA is the agent.

Plant organs (root, stem, leaf) are built from three tissue systems that handle protection, support, and transport.

Dermal tissue: epidermis, cuticle, stomata with guard cells (gas exchange). Ground tissue: parenchyma (photosynthesis/storage), collenchyma (flexible support), sclerenchyma (rigid support). Vascular tissue: xylem (water/mineral transport, dead cells at maturity), phloem (sugar transport, living cells). Roots anchor and absorb; stems support and transport; leaves photosynthesize via mesophyll layers.

Xylem (water/minerals move upward, one-way, dead at maturity) vs.\ phloem (sugars move bidirectionally source-to-sink, living cells).

Assuming stomata are always open --- guard cells close stomata to limit water loss under drought stress, regulated by turgor pressure and abscisic acid.

Xylem = water up (dead); phloem = sugar source$arrow$sink (alive).

Water moves passively up the plant via cohesion-tension driven by transpiration; sugars move actively by pressure flow.

Cohesion-tension theory: transpiration at the leaf creates tension; water's cohesion (hydrogen bonding) pulls a continuous column up the xylem. Pressure-flow (mass flow) hypothesis: sugar loaded at the source raises solute concentration, water follows osmotically, and bulk flow pushes sap toward the sink where sugar is unloaded.

Cohesion-tension (drives xylem water transport, passive, powered by evaporation) vs.\ pressure-flow (drives phloem sugar transport, requires active loading at the source).

Assuming phloem transport is always ``downward'' --- flow direction is source-to-sink, which can run upward or downward depending on which organ is currently the source vs.\ the sink.

Xylem pulled by transpiration (cohesion-tension); phloem pushed by pressure flow (source $arrow$ sink).

All plants alternate between a multicellular diploid sporophyte and a multicellular haploid gametophyte, with dominance shifting across plant lineages.

Ferns: dominant sporophyte, free-living gametophyte, water required for fertilization. Conifers: dominant sporophyte, reduced gametophyte (pollen = male; ovule contains female gametophyte), no water needed. Angiosperms: double fertilization --- one sperm + egg $arrow$ zygote, one sperm + two polar nuclei $arrow$ triploid endosperm; flower parts include stamen (anther/filament) and carpel (stigma/style/ovary).

Gametophyte (haploid, produces gametes by mitosis) vs.\ sporophyte (diploid, produces spores by meiosis).

Forgetting double fertilization is unique to angiosperms, producing both the zygote AND the triploid (3n) endosperm in a single event.

Sporophyte (2n, meiosis $arrow$ spores) $leftharpoons$ Gametophyte (n, mitosis $arrow$ gametes); angiosperms: double fertilization $arrow$ zygote + 3n endosperm.

Plant hormones coordinate growth responses to environmental stimuli and developmental timing without a nervous system.

Auxin (apical dominance, phototropism, cell elongation); gibberellins (stem elongation, seed germination); cytokinins (cell division, delay senescence); abscisic acid (stomatal closure, dormancy, stress response); ethylene (fruit ripening, abscission). Tropisms (phototropism, gravitropism, thigmotropism) result from differential auxin distribution causing differential cell elongation. Photoperiodism (flowering timing) is detected via the phytochrome pigment.

Phototropism (bending toward light, auxin-mediated) vs.\ photoperiodism (flowering timing response to day/night length, phytochrome-mediated).

Assuming ``short-day plants'' respond directly to day length --- they actually respond to night length (a critical uninterrupted dark period), a classic reversal trap.

Auxin bends shoots to light; phytochrome tracks night length for flowering.

Digestive and respiratory systems maximize surface area to make nutrient absorption and gas exchange efficient.

Digestion: mouth (amylase) $arrow$ esophagus $arrow$ stomach (pepsin, HCl) $arrow$ small intestine (villi/microvilli, main absorption site; bile and pancreatic enzymes) $arrow$ large intestine (water reabsorption). Respiration: gills (countercurrent exchange in fish), tracheae (insects, direct diffusion to tissues), lungs (alveoli, mammals); gas exchange follows diffusion down partial-pressure gradients.

Mechanical digestion (physical breakdown) vs.\ chemical digestion (enzymatic breakdown into absorbable monomers) --- both occur simultaneously in the stomach, not sequentially.

Treating all gas-exchange surfaces as equally efficient --- countercurrent exchange in fish gills (blood and water flow in opposite directions) sustains a diffusion gradient across the entire surface and is far more efficient than concurrent flow.

Gills = countercurrent; alveoli = huge surface area + thin, moist membrane.

Closed circulatory systems and the nephron allow precise, high-pressure control of internal fluid composition.

Open circulatory system (insects; hemolymph bathes tissues, low pressure) vs.\ closed (vertebrates; blood confined to vessels, higher pressure/efficiency). Heart chambers increase with metabolic demand: 2-chambered fish, 3-chambered amphibian/reptile, 4-chambered bird/mammal (separates oxygenated and deoxygenated blood). Nephron is the kidney's functional unit: filtration (Bowman's capsule), reabsorption (proximal/distal tubule, loop of Henle concentrates urine via a countercurrent multiplier), secretion, forming urine.

Open circulatory system (hemolymph directly bathes tissues) vs.\ closed circulatory system (blood stays in vessels) --- ``open'' does not mean the animal lacks a heart.

Assuming 4-chambered hearts occur only in mammals --- birds also have fully separated 4-chambered hearts, a frequently missed exception.

Open = hemolymph bathes tissue; closed = blood in vessels. Nephron: filter $arrow$ reabsorb $arrow$ secrete $arrow$ excrete.

Neurons transmit electrochemical signals via action potentials; hydrostatic, exo-, and endoskeletons provide support and movement through antagonistic muscle pairs.

Neuron: resting potential ($$$-$70 mV, K$^+$ leak channels, Na$^+$/K$^+$ pump); depolarization (Na$^+$ influx) triggers an all-or-none action potential; repolarization (K$^+$ efflux); saltatory conduction at Nodes of Ranvier speeds myelinated axons; synapses release neurotransmitter to the next cell. Skeletons: hydrostatic (fluid-filled cavity, e.g., earthworms), exoskeleton (external, chitin in arthropods, must molt to grow), endoskeleton (internal, bone/cartilage, grows with the organism). Muscles work in antagonistic pairs (flexor/extensor) because they can only contract.

Depolarization (Na$^+$ rushes in, potential becomes more positive) vs.\ repolarization (K$^+$ rushes out, potential returns toward resting).

Assuming muscles can ``push'' --- muscles only pull via contraction; extension requires an antagonistic muscle (e.g., triceps extends what the biceps flexed).

Na$^+$ in = depolarize; K$^+$ out = repolarize. Muscles only pull --- antagonistic pairs create movement.

The immune system layers nonspecific and specific defenses to distinguish self from non-self, while homeostasis mostly relies on negative feedback to keep internal conditions stable.

Innate immunity: physical barriers, phagocytes, inflammation, fever --- nonspecific, immediate. Adaptive immunity: humoral (B cells $arrow$ antibodies, targets extracellular pathogens) vs.\ cell-mediated (T cells --- helper T coordinate, cytotoxic T kill infected cells directly); has memory. Homeostasis: negative feedback opposes the stimulus (e.g., thermoregulation, insulin/glucagon control of blood glucose) and is by far the most common mechanism; positive feedback amplifies the stimulus (e.g., childbirth, blood clotting) and is comparatively rare.

Humoral immunity (B cells, antibody-mediated) vs.\ cell-mediated immunity (T cells, direct killing of infected/cancerous cells).

Assuming all physiological feedback is negative --- positive feedback loops (oxytocin during labor, depolarization during an action potential) intensify rather than reverse the stimulus.

Negative feedback = restore balance (most homeostasis); positive feedback = amplify (labor, clotting).

The endocrine system uses hormones for slower, longer-lasting regulation than the nervous system, typically through antagonistic pairs and feedback loops.

Hypothalamus-pituitary axis controls most other glands. Insulin (lowers blood glucose, promotes storage) vs.\ glucagon (raises blood glucose, promotes breakdown) --- an antagonistic pair. Thyroxine sets metabolic rate; FSH/LH drive gametogenesis and sex-hormone production; estrogen/progesterone regulate the female reproductive cycle; testosterone drives male reproductive development. Steroid hormones (lipid-soluble, cross the membrane, bind intracellular receptors) vs.\ peptide hormones (bind surface receptors, trigger second-messenger cascades).

Steroid hormones (diffuse through the membrane, act on gene transcription directly) vs.\ peptide hormones (bind a surface receptor, act via second messengers like cAMP).

Swapping insulin and glucagon's direction of effect --- insulin LOWERS blood glucose, glucagon RAISES it; a frequent reversal under time pressure.

Insulin lowers sugar (stores); glucagon raises sugar (releases). Steroid = through membrane; peptide = surface receptor.

Sexual reproduction combines haploid gametes from two parents via fertilization to restore diploidy and generate genetic variation.

Spermatogenesis produces 4 functional haploid sperm per meiosis; oogenesis produces 1 functional egg plus polar bodies, with unequal cytoplasm division. External fertilization (aquatic, many gametes, little parental contact) vs.\ internal fertilization (terrestrial adaptation, protects gametes from desiccation, typically fewer offspring with greater parental investment). Fertilization triggers the cortical reaction (blocks polyspermy) and completion of meiosis in the egg.

Spermatogenesis (4 equal haploid sperm per primary spermatocyte) vs.\ oogenesis (1 large egg + 2--3 small polar bodies per primary oocyte).

Assuming external fertilization is evolutionarily ``inferior'' --- it is an adaptation to aquatic environments, with high gamete output compensating for lower fertilization/survival probability.

Sperm: 4 equal cells; egg: 1 big cell + polar bodies. External = aquatic/many gametes; internal = terrestrial/fewer, protected.

Early animal development proceeds through a conserved sequence --- cleavage, gastrulation, organogenesis --- that establishes the body plan from three germ layers.

Cleavage: rapid mitotic divisions without growth, forms the blastula (hollow ball with a blastocoel). Gastrulation: cell movements form ectoderm (skin, nervous system), mesoderm (muscle, skeleton, circulatory system, most organs), and endoderm (digestive/respiratory lining), producing the gastrula with an archenteron. Organogenesis: germ layers differentiate into organs and systems (e.g., the notochord induces the neural tube from ectoderm in chordates).

Ectoderm (outer layer $arrow$ skin, nervous system) vs.\ endoderm (inner layer $arrow$ gut/respiratory lining) vs.\ mesoderm (middle layer $arrow$ muscle, skeleton, circulatory/excretory organs).

Assuming the nervous system must come from mesoderm because it lies deep in the body --- the brain and spinal cord actually derive from ectoderm via neurulation.

Ecto = skin + nerves; Meso = muscle/skeleton/circulatory; Endo = gut/lung lining.

Amniotes evolved extraembryonic membranes that free reproduction from standing water, and mammals further modified these into the placenta.

Amnion: fluid-filled protective sac cushioning the embryo. Chorion: outermost membrane, primary gas-exchange interface, contributes to the mammalian placenta. Yolk sac: nutrition (often vestigial in mammals, but forms the first blood cells). Allantois: waste storage/gas exchange, contributes to umbilical cord vessels in mammals. Placenta forms from chorion plus uterine tissue and exchanges nutrients, gases, and wastes between mother and fetus.

Amnion (fluid-filled sac protecting/cushioning the embryo) vs.\ chorion (outer membrane, main gas-exchange role, contributes most directly to the placenta).

Assuming maternal and fetal blood mix directly in the placenta --- they stay separated by membranes, with exchange occurring by diffusion and active transport, not direct mixing.

Amnion = cushion; chorion = gas exchange/placenta; yolk sac = nutrition; allantois = waste/cord vessels.

Mendel's laws of segregation and independent assortment explain how discrete hereditary factors pass from parents to offspring in predictable ratios.

Law of Segregation: allele pairs separate during gamete formation, so each gamete gets one allele. Law of Independent Assortment: genes on different chromosomes (or far apart on the same one) assort independently. Monohybrid cross Aa $×$ Aa $arrow$ 3:1 phenotypic ratio. Dihybrid cross AaBb $×$ AaBb $arrow$ 9:3:3:1 ratio. Test cross (unknown genotype $×$ homozygous recessive) reveals whether the unknown is homozygous or heterozygous dominant.

Genotype (allele combination, e.g., Aa) vs.\ phenotype (observable trait) --- monohybrid genotype ratio is 1:2:1, but the phenotype ratio is 3:1 under complete dominance.

Applying independent assortment to linked genes --- genes close together on the same chromosome do NOT assort independently and skew the expected dihybrid ratio unless separated by crossing over.

Segregation $arrow$ 1 allele per gamete; independent assortment $arrow$ 9:3:3:1 (dihybrid, unlinked genes).

Genes on the same chromosome are physically linked and inherited together unless separated by crossing over; sex-linked genes follow distinctive inheritance patterns.

Linked genes tend to be inherited together; recombination frequency (from crossing over) is used to map relative gene distance --- higher recombination frequency means genes are farther apart. Sex determination in mammals: XX (female)/XY (male). Males (XY) are hemizygous for X-linked genes --- a single recessive allele on their one X is expressed. Classic X-linked recessive examples: red-green color blindness, hemophilia --- both more common in males.

Autosomal recessive inheritance (equal likelihood in males and females, requires two copies) vs.\ X-linked recessive inheritance (far more common in males, who need only one copy).

Assuming a father can pass an X-linked trait directly to a son --- sons get the Y chromosome from their father and the X from their mother, so fathers pass X-linked traits only to daughters.

Higher recombination frequency = farther apart on the chromosome. Males are hemizygous for X --- X-linked recessive traits skip generations via carrier mothers.

Not every trait follows simple single-gene dominant/recessive patterns --- polygenic traits and multiple-allele systems produce continuous variation or more than two phenotype classes.

Polygenic inheritance: multiple genes contribute additively to one phenotype (e.g., human height, skin color), producing continuous, bell-curve variation. Multiple alleles: a gene with more than two allele variants across the population (though each individual still carries only 2) --- ABO blood groups ($I^A$, $I^B$, $i$; $I^A$ and $I^B$ codominant, both dominant to $i$) give 4 phenotypes from 6 genotypes. Incomplete dominance: heterozygote shows a blended intermediate phenotype (e.g., pink from red $×$ white). Codominance: both alleles are fully, separately expressed (e.g., AB blood type).

Incomplete dominance (heterozygote phenotype BLENDS, e.g., pink) vs.\ codominance (heterozygote phenotype shows BOTH traits fully and separately, e.g., AB blood type).

Assuming ``multiple alleles'' means one individual carries more than two alleles --- an individual still carries only two (one per homolog); ``multiple'' refers to the number of variants across the population's gene pool.

ABO: $I^A$/$I^B$ codominant, both dominant over $i$ $arrow$ 4 phenotypes. Incomplete dominance blends; codominance shows both.

Energy flows one-way through an ecosystem and is progressively lost as heat, while chemical matter cycles repeatedly between organisms and the environment.

Trophic levels: producers (autotrophs) $arrow$ primary consumers $arrow$ secondary consumers $arrow$ tertiary consumers; only about 10% of energy transfers to the next level (the rest lost as heat, per the second law of thermodynamics), which limits food-chain length and shapes energy pyramids. Biogeochemical cycles: carbon (photosynthesis/respiration, combustion, ocean-atmosphere exchange), nitrogen (nitrogen fixation converts N$_2$ to usable forms; nitrification; denitrification returns N$_2$ to the atmosphere), water (evaporation, transpiration, precipitation).

Energy flow (one-way through trophic levels, lost as heat, continually resupplied by the sun) vs.\ nutrient/matter cycling (recycled repeatedly through biotic and abiotic reservoirs, not lost).

Assuming energy pyramids and biomass pyramids always share the same shape --- some aquatic ecosystems show inverted biomass pyramids (fast-turnover phytoplankton supporting more zooplankton biomass at any instant) even though energy pyramids are always upright.

Energy: one-way, $$10% per level, lost as heat. Matter: cycles (C, N, H$_2$O) through biogeochemical pathways.

Populations grow exponentially under unlimited resources but are constrained by carrying capacity and density-dependent factors in real environments.

Exponential growth: $/dNdt = rN$ (J-shaped curve, unlimited resources). Logistic growth: $/dNdt = rN≤ft(/K-NK)$ (S-shaped curve, growth slows as N approaches carrying capacity K). Density-dependent factors (competition, predation, disease --- intensify with density) vs.\ density-independent factors (natural disasters, climate). r-selected species (small, fast-reproducing, many offspring, little parental care) vs.\ K-selected species (large, slow-reproducing, few offspring, high parental care, near carrying capacity).

r-selected strategy (maximize reproductive rate $r$, e.g., insects, weeds) vs.\ K-selected strategy (maximize competitiveness near carrying capacity $K$, e.g., elephants, humans).

Assuming population growth in nature is always exponential --- real populations experience logistic growth as resources become limiting, and a leveling S-curve must be identified as logistic, not exponential.

Exponential: $dN/dt=rN$ (J-curve); logistic: $dN/dt=rN(K-N)/K$ (S-curve, levels at K).

Species interactions and disturbance history structure communities over time, moving them predictably toward a relatively stable climax community.

Interactions: competition ($-/-$), predation ($+/-$), parasitism ($+/-$), mutualism ($+/+$), commensalism ($+/0$). Competitive exclusion principle: two species competing for the identical limiting resource cannot coexist indefinitely. Primary succession: starts on bare rock with no soil (e.g., after glacier retreat), pioneer species like lichens, very slow. Secondary succession: starts where soil already remains after a disturbance (e.g., fire, abandoned farmland), much faster.

Primary succession (no pre-existing soil, begins with pioneer species, very slow) vs.\ secondary succession (soil already present, faster recovery).

Confusing parasitism with predation --- parasitism typically does not kill the host immediately and the parasite persists on/in the host, while predation involves the predator killing and consuming the prey outright.

Primary succession = no soil, starts from scratch (lichens); secondary = soil intact, faster.

Global biome distribution reflects temperature and precipitation patterns, while niche theory and island biogeography explain species coexistence and diversity.

Major terrestrial biomes: tropical rainforest, savanna, desert, temperate grassland, temperate forest, taiga (boreal forest), tundra --- distinguished by temperature and precipitation. Niche = the full range of biotic/abiotic conditions and resources a species uses; fundamental niche (potential range) vs.\ realized niche (actual range once competitors are present). Island biogeography theory: species richness reflects equilibrium between immigration rate (falls as the island fills) and extinction rate (rises with fewer species/smaller populations); larger and closer islands support more species.

Fundamental niche (the full range a species COULD occupy absent competition) vs.\ realized niche (the range it actually DOES occupy once competitors narrow it).

Assuming island size and distance from the mainland drive richness through the same mechanism --- larger islands lower extinction rate (more resources), while closer islands raise immigration rate; the exam may ask which factor drives which process.

Fundamental niche (could) narrows to realized niche (does, due to competition). Island biogeography: bigger + closer = more species.

Natural selection changes allele frequencies when there is heritable variation in fitness; the Hardy-Weinberg equation models a non-evolving population as the null hypothesis for detecting evolution.

Requirements for natural selection: variation, heritability, differential reproductive success. Hardy-Weinberg: $p + q = 1$ and $p^2 + 2pq + q^2 = 1$, where $p$ = dominant allele frequency, $q$ = recessive allele frequency, $p^2$ = homozygous dominant frequency, $2pq$ = heterozygous frequency, $q^2$ = homozygous recessive frequency. Five conditions required for equilibrium (no evolution): no mutation, no gene flow, infinitely large population (no drift), random mating, no selection. Modes of selection: directional (shifts the mean toward one extreme), stabilizing (favors the intermediate, reduces variation), disruptive (favors both extremes).

Directional selection (favors one extreme, shifts the population mean) vs.\ disruptive selection (favors BOTH extremes over the intermediate, can split the phenotype distribution).

Forgetting to take the square root of $q^2$ to find $q$ when given only the recessive phenotype frequency --- a very common computational slip in Hardy-Weinberg problems.

$p+q=1$; $p^2+2pq+q^2=1$. Violate any of the 5 HW conditions $arrow$ the population evolves.

Speciation occurs when populations become reproductively isolated and accumulate enough genetic divergence that they can no longer interbreed.

Allopatric speciation: geographic separation prevents gene flow (most common mode). Sympatric speciation: new species arise without geographic separation, e.g., via polyploidy in plants. Prezygotic isolation (habitat, temporal, behavioral, mechanical, gametic --- prevent mating/fertilization) vs.\ postzygotic isolation (hybrid inviability, sterility, breakdown --- act after fertilization). Punctuated equilibrium: the fossil record shows long stasis punctuated by relatively rapid bursts of speciation, contrasting with gradualism (slow, continuous change).

Prezygotic isolation (barriers preventing mating or fertilization) vs.\ postzygotic isolation (barriers acting after fertilization, e.g., sterile hybrids like mules).

Treating punctuated equilibrium as contradicting natural selection --- it is a hypothesis about the fossil record's tempo (rapid bursts plus long stasis), not an alternative mechanism to selection.

Allopatric = geography splits them; sympatric = no geographic split (e.g., polyploidy). Punctuated equilibrium = stasis + rapid bursts, not gradual.

Comparative anatomy, molecular biology, and observed population genetics converge as independent lines of evidence for evolution by descent with modification.

Homologous structures (similar structure, common ancestry, e.g., vertebrate forelimbs) vs.\ analogous structures (similar function, no common ancestry, convergent evolution, e.g., insect wings vs.\ bird wings). Vestigial structures are reduced remnants of ancestrally functional structures (e.g., the human appendix). Genetic drift: random allele-frequency change, stronger in small populations; bottleneck effect (sudden crash randomly reduces diversity) and founder effect (small group establishes a new isolated population with unrepresentative allele frequencies). Balanced polymorphism: multiple phenotypes maintained via heterozygote advantage (e.g., the sickle-cell allele confers malaria resistance in heterozygotes).

Homologous structures (shared ancestry, e.g., human arm/bat wing/whale flipper) vs.\ analogous structures (shared function only, via convergence, e.g., bird wing and butterfly wing).

Confusing the bottleneck effect (sudden crash in an EXISTING population) with the founder effect (a small subset breaks off to found a NEW, isolated population) --- both reduce diversity via drift but arise differently.

Homologous = same structure/ancestry; analogous = same function/convergent. Bottleneck = crash in place; founder = small group starts anew.

Modern classification organizes life into a nested hierarchy that increasingly reflects evolutionary relationships (phylogeny) rather than superficial similarity alone.

Linnaean hierarchy (broad to narrow): Domain, Kingdom, Phylum, Class, Order, Family, Genus, Species. Three domains: Bacteria, Archaea, Eukarya. Traditional kingdoms within Eukarya: Protista, Fungi, Plantae, Animalia. Binomial nomenclature: Genus species (italicized, genus capitalized). Phylogenetic trees/cladograms depict evolutionary relationships based on shared derived characters (synapomorphies).

Overall resemblance (used in older phenetic classification) vs.\ shared derived characters/synapomorphies (used in modern cladistics, based on evolutionary relatedness) --- cladistics can group organisms that look different but share a recent common ancestor.

Listing taxonomic ranks out of order --- remember ``Dear King Philip Came Over For Good Soup'' (Domain, Kingdom, Phylum, Class, Order, Family, Genus, Species); swapping Family/Genus or Order/Class is a common slip.

Domain > Kingdom > Phylum > Class > Order > Family > Genus > Species (``Dear King Philip Came Over For Good Soup'').

Humans share a relatively recent common ancestor with other primates, and the hominin fossil record documents a branching, mosaic pattern of trait acquisition, not a straight line.

Humans (Homo sapiens) belong to order Primates, family Hominidae; closest living relatives are chimpanzees. Key hominin trends: bipedalism arose well before large brain size (e.g., Australopithecus was bipedal with an ape-sized brain); cranial capacity progressively increased through Homo habilis and Homo erectus to Homo sapiens, alongside tool use and eventually complex culture and language. Multiple hominin species coexisted at various points --- the record is a branching tree, not a ladder.

Human evolution is NOT a linear ``ladder'' from ape to human --- it is a branching phylogenetic tree with multiple coexisting hominin species, most of which did not lead to modern humans.

Assuming brain size expanded before or alongside bipedalism --- fossils such as Australopithecus afarensis (``Lucy'') show bipedalism evolved well before significant brain enlargement.

Bipedalism before big brains. Human evolution = branching bush, not a straight ladder.

Behavior ranges from fixed, innate patterns shaped by natural selection to flexible, learned responses shaped by individual experience.

Innate behavior: fixed action patterns (FAPs) --- triggered by a specific sign stimulus, run to completion once started, largely genetically programmed. Learned behavior: habituation (decreased response to a repeated harmless stimulus), classical conditioning (associating a neutral stimulus with a significant one), operant conditioning (behavior shaped by reward/punishment), imprinting (rapid learning during a critical period, e.g., filial imprinting in birds). Social behavior: altruism (benefits another at a cost to self) explained by kin selection (helping relatives who share genes) and inclusive fitness; eusociality documented in insects (bees, ants), birds, and primates.

Classical conditioning (passive association between two stimuli, involuntary response) vs.\ operant conditioning (active behavior shaped by its consequences).

Assuming altruism contradicts natural selection because of its individual fitness cost --- kin selection resolves this: helping close relatives who share alleles can raise inclusive fitness even at a personal cost.

FAP = fixed, sign stimulus triggers, runs to completion. Kin selection $arrow$ altruism can still raise inclusive fitness.

Human populations follow the demographic transition model as societies industrialize, and human activity increasingly drives environmental and biomedical change.

Demographic transition: Stage 1 (high birth and death rates, slow growth, pre-industrial); Stage 2 (death rate falls due to sanitation/medicine, birth rate stays high --- rapid growth); Stage 3 (birth rate begins falling, industrializing); Stage 4 (low birth and death rates, stable, developed). Age-structure diagrams predict future growth: broad-based pyramid = expanding, columnar = stable, top-heavy = declining. Human environmental impacts: resource depletion, pollution, habitat loss. Biomedical advances: reproductive technology, genetic engineering (recombinant DNA, gene therapy).

Stage 2 of demographic transition (DEATH rate falls first, driving the population boom) vs.\ Stage 3 (BIRTH rate finally begins falling).

Assuming a broad-based, pyramid-shaped age structure signals population decline --- a wide young base actually predicts future GROWTH as those individuals reach reproductive age.

DT stages: (1) high-high, (2) death$$, birth stays high $arrow$ boom, (3) birth$$, (4) low-low, stable.

$p^2+2pq+q^2=1$ and $dN/dt=rN(K-N)/K$ are the two equations CLEP most often asks you to apply.

Three domains split first on cell type (pro- vs.\ eukaryotic) and biochemistry, not on ``plant vs.\ animal.''

If a question names an experiment, it is testing whether you know WHAT that experiment proved, not just its date.

Genotype from the cross $arrow$ phenotype from the dominance rule $arrow$ inheritance mode from the pattern across generations.

115 questions, 90 minutes, all multiple choice, no essay --- pace yourself at well under a minute per question.

Promoter $arrow$ pre-mRNA $arrow$ processed mRNA $arrow$ ribosome $arrow$ polypeptide $arrow$ folded, targeted protein.

$q^2arrow q$ (square root) $arrow p=1-q arrow$ plug both into $p^2+2pq+q^2=1$.