Fall 2025 • Biology Finals← Back to review hub

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Finals Cheat Sheet Hub

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Built straight from your Fall Finals Cheat Sheet Guide. Use this as a condensed dashboard to redraw or jot onto your allowed handwritten pages.

Exam format

  • • 85 MCQ, no FRQ
  • • 5 pages handwritten (front/back), 8.5x11
  • • Old Unit 3 & 5 sheets allowed

Immediate focus

  • • Five handwritten pages (front + back) allowed; prior Unit 3/5 sheets usable.
  • • 85 MCQ, no FRQ. Bring focused, high-yield reminders over paragraphs.
  • • Review older assignments + labs; replicate key figures (membranes, mitochondria, signaling cascades).
  • • Translate tricky visuals (isomers, tone of pH, ETC) into quick cues you can redraw fast.

Study Moves (do now)

  • ✓Redraw pathways from memory: glycolysis → ETC, signaling cascades, action potential stages.
  • ✓Flash-quiz vocabulary (ligand, second messenger, ∆G, tonicity) to lock definitions.
  • ✓Practice data analysis: interpret error bars (SEM×2), identify proper controls, predict outcomes.
  • ✓Link structure to function: how saturation changes fluidity; why enzymes lower Ea but not ∆G.
  • ✓Do timed MCQ sets: 85 Q scope → aim for <1 min/Q; mark and move if stuck.

Scroll for unit deep dives

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Unit Summary

Unit 1 • Chemistry of Life

Essentials: bonds, macromolecules, pH, experimental design

High yield

Bonds & Strength

Hydrogen

Weak attraction between partial charges (e.g., between water molecules or DNA bases); easily broken for flexibility.

Ionic

Electrostatic attraction between charged ions; strong in dry environments, weaker in aqueous cytosol.

Covalent

Shared electron pair; strongest in cells and forms backbones of macromolecules (peptide, glycosidic, phosphodiester).

Van der Waals

Transient interactions between fluctuating charges; stabilize hydrophobic packing (lipid tails, protein cores).

Macromolecules

Carbohydrate

C, H, O

Monosaccharide (CnH2nOn) • Polysaccharides (starch, glycogen, cellulose)

Short-term energy, structure (cellulose), recognition (glycoproteins). Glycosidic bonds via dehydration; hydrolysis releases energy.

Lipid

C, H, O

No single monomer; fatty acids + glycerol backbone • Triglycerides, phospholipids, steroids, waxes

Long-term energy storage, membranes (amphipathic bilayers), hormones, insulation. Hydrophobic interactions drive bilayer formation.

Protein

C, H, O, N (±S)

Amino acid (central C, amine, carboxyl, R-group) • Polypeptides (enzymes, motors, receptors)

Catalysis, signaling, transport, structure, motion. Shape depends on primary sequence + H-bonds/ionic/hydrophobic forces.

Nucleic Acid

C, H, O, N, P

Nucleotide (sugar, phosphate, N-base) • DNA, RNA

Genetic storage, information transfer, catalysis (ribozyme), short-term energy (ATP). Phosphodiester bonds form sugar-phosphate backbone.

pH Math + Tips

pH = -log[H⁺] • pOH = -log[OH⁻] • pH + pOH = 14.

  • 0–7 acidic → higher [H⁺]; strong acids fully ionize.
  • 7 neutral → [H⁺] = [OH⁻] (water).
  • 7–14 basic → higher [OH⁻]; household bases near 13-14.
  • Each pH unit = 10× change in [H⁺]; buffers resist swings (weak acid/base + conjugate).

Practice: convert pH ↔ [H⁺]; sketch titration curve labels (pKa = half-equivalence).

Experimental Design

Positive control

Confirms the system can show an effect (validates detection works).

Negative control

Baseline with no treatment; expects no effect to reveal background noise.

Independent variable

Factor intentionally changed between groups.

Dependent variable

Measured response that depends on the independent variable.

Control variables

Kept constant to isolate the tested factor.

Standard deviation

Spread around mean; bigger SD = more variability.

SEM / SEM×2

Mean accuracy; SEM×2 approximates 95% CI. Non-overlap suggests real difference.

Error bars

Usually SEM or CI; overlapping bars hint at non-significant difference.

Isomers

Structural

Different covalent arrangement (e.g., chain vs branched); different properties.

Cis-trans

Same covalent bonds, differ around double bond (cis = same side, trans = opposite).

Enantiomer

Mirror images; not superimposable (L vs D amino acids).

Unit Summary

Unit 2 • Cell Structure & Membranes

Cells, transport, signaling, membranes

High yield

Eukaryote vs Prokaryote

Eukaryotes: membrane-bound organelles, linear chromosomes, mitosis/meiosis, larger (10–100 µm).

Prokaryotes: no nucleus, circular DNA in nucleoid, plasmids common, smaller (0.1–5 µm), binary fission.

Surface area/volume matters: smaller cells exchange materials faster relative to volume.

Fluid Mosaic & Temperature

  • Unsaturated (cis) tails → more fluid; useful in cold to prevent solidification.
  • Saturated tails → less fluid; useful in heat to avoid melting/disruption.
  • Cholesterol buffers: prevents solid in cold, prevents excess fluid in heat.
  • Integral proteins span bilayer; peripheral proteins loosely attached; glycolipids/glycoproteins for recognition.

Key Organelles

Nucleus

Houses DNA; nucleolus builds rRNA and ribosomal subunits; double membrane with pores.

Ribosome

Protein synthesis; free → cytosolic proteins, bound (RER) → secretion/membranes.

Mitochondria

Aerobic respiration; cristae hold ETC/ATP synthase, matrix hosts link + Krebs.

Lysosome

Acidic hydrolases for recycling + apoptosis; optimized at low pH.

Rough ER

Protein folding, glycosylation; membrane + secreted proteins.

Smooth ER

Lipid synthesis, detox, Ca²⁺ storage (muscle SR).

Golgi

Protein modification/sorting; cis → trans stack; ships vesicles.

Cytoskeleton

Microtubules (tracks/mitosis), microfilaments (shape, movement), IFs (tension).

Fluid Mosaic

Dynamic bilayer with proteins, cholesterol; unsaturated tails increase fluidity.

Signaling Vocabulary

Ligand

Signal molecule that binds a receptor (peptide, steroid, ion).

Reception

Ligand binds receptor (GPCR, RTK, ion channel); shape change starts cascade.

Transduction

Multi-step relay (kinase cascades, phosphorylation, second messengers).

GPCR

Activates G-protein → GTP; triggers effectors (adenylyl cyclase, ion channels).

Second messenger

Small, fast signals (cAMP, IP3, Ca²⁺); amplify extracellular message.

Kinase / phosphatase

Kinase adds phosphate to activate/inactivate; phosphatase removes to reset.

Diffusion & Transport

Simple diffusion

Small/nonpolar down gradient; no protein, no energy.

Facilitated diffusion

Polar/charged down gradient via channel or carrier; no ATP.

Active transport

Against gradient; needs ATP or coupled gradient (pumps, symporters, antiporters).

Hypertonic

Higher solute outside; cell loses water → shrivels/crenates (plants: plasmolysis).

Hypotonic

Lower solute outside; cell gains water → swells (plants: turgid, animals risk lysis).

Isotonic

Equal solute; no net water change, best for animal cells.

Unit Summary

Unit 3 • Homeostasis, Neurons, Muscles

Feedback loops, action potentials, quorum sensing

High yield

Homeostasis Vocabulary

Homeostasis

Maintaining internal balance (temp, pH, glucose) despite external change.

Negative feedback

Counteracts change to return to set point (thermoregulation, blood glucose with insulin/glucagon).

Positive feedback

Amplifies change (oxytocin during birth, platelet plug formation).

Feedback inhibition (enzymes)

End product allosterically inhibits an earlier enzyme to prevent overproduction.

Action Potential Sequence

1

Rest: leak K⁺ + Na⁺/K⁺ pump keep -70 mV.

2

Threshold reached: ligand-gated or graded potentials depolarize membrane.

3

Voltage-gated Na⁺ channels open → rapid depolarization.

4

Na⁺ channels inactivate; voltage-gated K⁺ channels open → repolarization.

5

K⁺ efflux overshoots (hyperpolarization); pump + leak reset resting potential.

Ionotropic = ligand-gated ion channels (fast). Metabotropic = GPCR → second messengers (slower, amplified).

Muscle & Sliding Filament

  • Structure: muscle → fascicle → fiber → myofibril → sarcomere (actin thin, myosin thick).
  • Sliding filament: Ca²⁺ from SR binds troponin → tropomyosin shifts → myosin heads bind actin → power stroke (ATP → ADP + Pi).
  • ACh at neuromuscular junction depolarizes muscle → AP travels T-tubules → Ca²⁺ release.

Quorum Sensing

Bacteria communicate with autoinducers; when signal crosses threshold, community genes turn on (biofilms, virulence, light emission).

Species-specific and interspecies signals exist; density-dependent regulation is key theme.

Unit Summary

Unit 4 • Energetics & Respiration

Enzymes, ∆G, thermodynamics, respiration

High yield

Thermo & ∆G

1st Law: energy conserved. 2nd Law: every energy transfer increases entropy (disorder); some energy lost as heat.

∆G < 0 → spontaneous/exergonic/catabolic (energy released). ∆G > 0 → nonspontaneous/endergonic/anabolic (energy input).

ATP couples exergonic to endergonic by phosphorylation; phosphate transfer makes targets more reactive.

Enzymes

  • Lower Ea; do not change ∆G or equilibrium.
  • Factors: temperature, pH, substrate concentration, cofactors/coenzymes.
  • Regulation: allosteric activators/inhibitors, phosphorylation, feedback inhibition.

Respiration Flow

Remember redox: OIL RIG; reduced has H.
Glycolysis (cytosol): glucose → 2 pyruvate + 2 NADH + net 2 ATP.
Link reaction (matrix): pyruvate → acetyl-CoA + NADH + CO₂.
Citric acid cycle (matrix): per acetyl-CoA → 3 NADH + FADH₂ + GTP/ATP + 2 CO₂.
ETC + oxidative phosphorylation (inner membrane): electron flow pumps H⁺ to intermembrane space; ATP synthase uses gradient to make ATP (~26-28). O₂ is final e⁻ acceptor → H₂O.
Anaerobic: fermentation regenerates NAD⁺ (lactate or ethanol + CO₂); yields 2 ATP per glucose.

NAD⁺ → NADH

Reduced with H⁻; carries high-energy electrons to ETC (3 ATP per pair theoretical).

FAD → FADH₂

Enters ETC at complex II; yields ~2 ATP per pair theoretical.

Mitochondria Map

Inner membrane

Holds ETC complexes + ATP synthase; impermeable to ions → H⁺ gradient forms.

Matrix

Pyruvate oxidation + Krebs cycle enzymes, mtDNA, ribosomes.

Intermembrane space

Protons accumulate here during ETC; gradient drives ATP synthase back into matrix.

Anaerobes

Obligate cannot use O₂ (toxic); facultative switch between aerobic and fermentation.

Enzyme Inhibition

Competitive

  • • Binds active site; resembles substrate
  • • High substrate can outcompete
  • • Vmax unchanged; Km increases (need more substrate)

Noncompetitive/allosteric

  • • Binds other site → shape change
  • • Adding substrate cannot restore full rate
  • • Lowers effective enzyme concentration; Vmax drops

Unit Summary

Unit 5 • DNA & Expression

DNA basics, replication, cell cycle, cancer, viruses

High yield

DNA vs RNA

Sugar

DNA: deoxyribose (no 2' OH) → stable; RNA: ribose (2' OH) → reactive.

Bases

DNA: A, T, C, G; RNA: A, U, C, G.

Strands

DNA: double helix, antiparallel; RNA: mostly single-stranded, can fold into hairpins.

Role

DNA stores; RNA acts (mRNA, tRNA, rRNA, snRNA, miRNA) + catalysis (ribozyme).

Basic Nucleotide

Sugar (ribose/deoxyribose) + phosphate + nitrogenous base. Phosphodiester bond links 3' OH to 5' phosphate of next nucleotide → antiparallel strands with 5'→3' directionality.

Base pairing: A=T (2 H-bonds), C≡G (3 H-bonds). GC-rich regions have higher melting temps.

Viral Specificity & Origins

Host range

Viral surface proteins must match specific host cell receptors; defines species + tissue tropism.

Genome types

DNA or RNA, single- or double-stranded. RNA genomes rely on RNA polymerases (no host proofreading) → higher mutation.

Virus-first

Self-assembled before cells; independent origin.

Reductionist

Cells downsized under pressure; stripped genomes/proteins.

Escape

Escaped genes/cassettes acquired capsids and became parasites.

Key Viral Proteins

RdRp

RNA-dependent RNA polymerase copies RNA genome using RNA template; not encoded by host.

Reverse transcriptase

Makes DNA from viral RNA, inserts into host genome; error-prone.

Prions

  • • Protein-only; no nucleic acid.
  • • Misfolded β-sheet-rich proteins induce misfolding of normal proteins → aggregates.
  • • Aggregates kill neurons; resistant to heat/acid—no easy deactivation.

DNA Replication Essentials

1

Helicase unwinds; topoisomerase relieves supercoils ahead of fork.

2

Single-strand binding proteins stabilize unwound strands.

3

Primase lays RNA primers.

4

DNA polymerase III extends 5'→3' from primers (leading continuous; lagging Okazaki).

5

DNA polymerase I replaces RNA primers with DNA; ligase seals sugar-phosphate backbone.

6

Proofreading + mismatch repair correct errors; ligase finishes nicks.

Telomerase extends lagging strand ends (common in germline + cancer) to prevent shortening.

Central Dogma (Core Enzymes)

Transcription (nucleus): RNA polymerase binds promoter (with transcription factors) → mRNA.
RNA processing (euk): 5' cap, poly-A tail, splicing out introns.
Translation (cytosol/RER): ribosome reads mRNA; tRNAs bring amino acids; peptide bonds via peptidyl transferase.
Protein targeting: signal peptides send proteins to ER, mitochondria, or remain cytosolic.

RNA polymerase builds RNA 5'→3'. Ribosomes read mRNA codons (5'→3'); tRNA anticodons pair antiparallel.

Replication Enzymes (order)

1

Helicase: unwinds double helix.

2

SSB proteins: keep strands apart.

3

Primase: lays RNA primers.

4

DNA pol III: extends leading + lagging strands.

5

DNA pol I: replaces RNA primers with DNA.

6

Ligase: seals sugar-phosphate backbone.

Leading: one primer. Lagging: many primers + Okazaki fragments.

RNA Roles & Prok vs Euk

mRNA

Carries genetic message; codons specify amino acids; template for translation.

tRNA

Brings specific amino acid; anticodon pairs with mRNA codon.

rRNA

Ribosome catalyst; forms peptide bond; structural scaffold with proteins.

Transcription vs Translation

  • • Transcription in nucleus, translation in cytoplasm; linear chromosomes; mRNA processed (cap, tail, splicing); introns removed.
  • • Both in cytoplasm; circular DNA; no introns; transcription/translation coupled.

Gene Expression Control

DNA level

Methylation condenses/silences; histone acetylation opens chromatin → transcription.

Transcription factors

General (TATA-binding protein) vs specific (enhancer-binding activators/repressors).

Post-transcription

5' cap + poly-A tail for protection/export/ribosome binding; alternative splicing for isoforms.

Post-translation

Cleavage, phosphorylation, glycosylation, ubiquitin to change activity, location, stability.

ncRNA

miRNA/siRNA can degrade mRNA or block ribosome binding; lncRNA can alter chromatin.

Mutations & Translation Stops

Missense

Point mutation → new amino acid; impact depends on chemistry/position.

Nonsense

Point mutation → stop codon; truncates protein.

Silent

Point mutation → same amino acid; can still affect splicing/translation speed rarely.

Frameshift

Indel not multiple of 3 shifts reading frame → early stop, altered amino acids.

Stop codon → release factor (protein) terminates translation; tRNAs never carry stop anticodons. Degenerate code: several codons per amino acid, but one amino acid per codon.

DNA pol vs RNA pol

Direction built

Both synthesize 5'→3' and move along template 3'→5'.

Primer

DNA pol needs primer; RNA pol does not.

Proofreading

DNA pol proofreads; RNA pol lacks strong proofreading → more errors tolerated.

Helicase

DNA pol needs helicase; RNA pol can unwind small regions itself.

RNA pol error rate is higher but acceptable; DNA pol proofreads to protect genomes.

Checkpoints (fast recall)

G1

Checks size, nutrients, DNA damage; p53 can halt for repair or trigger apoptosis.

G2

Ensures DNA replication completed, damage repaired before mitosis.

M (spindle)

Verifies kinetochores attached to spindle before separating chromatids.

Cell Cycle & Checkpoints

G1: growth; G1/S checkpoint evaluates size, nutrients, DNA integrity.
S: DNA replication.
G2: prep for mitosis; G2/M checkpoint checks replication completion + DNA damage.
M: mitosis + cytokinesis; spindle checkpoint ensures proper kinetochore attachment.

Cyclins/CDKs drive transitions; p53 can pause cycle for repair or trigger apoptosis if damage persists.

Extras

  • • G1 size/nutrients/DNA damage; G2 replication complete; M spindle attachment.
  • • Programmed cell death if damage persists; cancer often evades.
  • • From centrosomes; attach kinetochores, align in metaphase, shorten in anaphase.
  • • Cohesin holds sisters; separase cleaves at anaphase; actin ring pinches in cytokinesis.
  • • Density-dependent inhibition; anchorage dependence.

Cancer & Viruses

Proto-oncogenes (e.g., Ras, Myc): gain-of-function mutations → uncontrolled growth signaling.
Tumor suppressors (e.g., p53, Rb, BRCA): loss-of-function disables checkpoints/repair.
Mutagens/carcinogens: radiation, chemicals, viruses increase mutation rate; telomerase reactivation supports immortality.

Cancer logic

  • • Growth-promoting; gain-of-function (dominant) mutations → stuck ON (e.g., Ras).
  • • Brake proteins; loss-of-function (recessive) mutations disable checkpoints (p53, Rb, BRCA).
  • • Normal cells stop with crowding or no attachment; cancer often ignores both.

Viruses

  • • Obligate intracellular; capsid ± envelope.
  • • Lytic: rapid replication → host lysis.
  • • Lysogenic: genome integrates (prophage/provirus); can later enter lytic.
  • • RNA viruses often use RNA-dependent RNA polymerase; retroviruses use reverse transcriptase → DNA → integration.
  • • Vaccines prime adaptive immunity; antivirals target entry, replication, assembly, or release.