BIOL 4230 Evolution — Cheat Sheet (L01-L20)

L01 · What Is Evolution? Course Intro

§A Defining evolution

Evolution = change in allele frequencies in a population over generations.
The unit of evolution is the population, not the individual.
Individuals are selected; populations evolve.
Heritable variation is required for evolutionary change to occur.

Evolution=change in heritable allele frequencies across generations·Population=interbreeding individuals of one species in an area·Heritable variation=genetic-basis trait differences passable to offspring

§B Why evolution unifies biology

Dobzhansky 1973: 'Nothing in biology makes sense except in the light of evolution.'
Explains both unity (common descent) and diversity (lineage-specific adaptations).
Applications: antibiotic resistance, vaccine design, conservation, crop improvement.

Common descent=all life shares an ancestor; similarity from inheritance·Adaptation=heritable trait raising fitness, made by selection

§C The four evolutionary mechanisms

Natural selection — non-random; differential survival/reproduction by trait variation.
Genetic drift — random sampling of alleles; strongest in small populations.
Gene flow — movement of alleles between populations; tends to homogenize.
Mutation — ultimate source of new variation; random with respect to fitness.

Natural selection=differential reproduction from heritable trait variation, non-random·Genetic drift=random allele-frequency change, esp. small N·Gene flow=allele movement between populations via migration·Mutation=heritable DNA change; ultimate source of new alleles

L02 · Evolutionary Thinking — Pre-Darwin to NS

§A Great Chain of Being / pre-Darwin

Great Chain of Being: fixed hierarchy with humans at apex.
Species assumed immutable; created in final form, not changing.
Extinction denied or downplayed well into the 1700s.
No concept of common ancestry — similarity meant shared design.

Great Chain of Being (Scala Naturae)=pre-Darwinian fixed ladder, no descent·Immutability=pre-Darwinian assumption species don't change

§B Extinction recognized — Smith

William Smith (early 1800s) used fossils + stratigraphy to map English rock layers.
Distinct fossil assemblages occur in consistent vertical order — faunal succession.
Disappearance of fossil types from younger strata established extinction as real.
Cuvier independently demonstrated extinction by comparing fossil to living mammals.

Stratigraphy=study of rock layers; younger atop older·Faunal succession=fossils occur in consistent vertical order; date rocks by fossils·Extinction=complete disappearance of a lineage

§C Lamarck, Lyell, road to Darwin

Lamarck (1809): inheritance of acquired characteristics — wrong on mechanism, right that species change.
Lyell: uniformitarianism — same gradual processes shaped Earth over deep time.
Lyell's gift to Darwin: deep time = millions/billions of years for slow change.

Lamarckism=traits gained in life pass to offspring (wrong)·Uniformitarianism=gradual processes over deep time shape Earth·Deep time=millions-billions of years over Earth history

§D Darwin, Wallace, natural selection

Darwin: Beagle voyage (1831-36); Galápagos finches; barnacles → natural selection.
Three obs + one inference: variation, overproduction, non-random survival → trait freq shift.
Wallace independently from Malay Archipelago; 1858 letter spurred Darwin to publish.
On the Origin of Species published 1859.

Natural selection=heritable variants raising reproduction become more common·Heritability=portion of phenotypic variance that is genetic·S (selection differential)=mean of breeders − mean of population

§E Hypothesis vs. theory

Hypothesis = tentative, testable, narrow explanation; designed to be falsified.
Scientific theory = broad, well-supported explanation; generates many hypotheses.
Evolution is a theory in the strong sense, supported by many evidence streams.
A good hypothesis is falsifiable — specifies what would prove it wrong.

Hypothesis=tentative, testable, falsifiable explanation·Scientific theory=broad well-supported explanation; spawns hypotheses·Falsifiability=specifies what observations would refute

L03 · Genes and Heritable Variation

§A Genome architecture — coding vs. noncoding

Protein-coding ~1-2% of human genome; bulk is noncoding.
Noncoding includes pseudogenes, transposons/retroelements, regulatory DNA, repeats.
Genome size does NOT correlate with complexity (C-value paradox).
Pseudogenes are evolutionary fossils — direct evidence of evolutionary history.

Pseudogene=nonfunctional sequence, broken by stops/frameshifts·MGE=DNA that changes position; transposons, LINEs, SINEs·C-value paradox=genome size ≠ complexity

§B Levels of gene expression regulation

Pre-transcriptional: chromatin, histone mods, DNA methylation — controls accessibility.
Transcriptional: TFs binding promoters/enhancers; rate of mRNA synthesis.
Post-transcriptional: alt. splicing, miRNA degradation, mRNA stability.
Post-translational: phosphorylation, ubiquitination, cleavage; alters made protein.

DNA methylation=methyl on CpG; usually represses; PRE-txn·Histone modification=acetyl/methyl on tails; alters chromatin; PRE-txn·miRNA=small RNA degrades mRNA; POST-txn·Alternative splicing=multiple mRNAs from one gene; POST-txn

§C Alleles — dominant, recessive, additive

Dominant alleles mask recessives in heterozygotes (Aa shows A).
Additive: each allele incremental; Aa intermediate; effect scales linearly.
Recessive beneficial mutations spread SLOWLY when rare (hidden in heterozygotes).
Dominant beneficial mutations spread FAST — every Aa shows phenotype.
V_A is the only variance component that responds predictably to selection.

Allele=variant of a gene at a locus·Dominant=fully expressed in heterozygote·Recessive=expressed only when homozygous·Additive=linear dose-response across copies·Locus=chromosomal location of a gene

§D Mutation as source of variation

Mutations are heritable DNA changes; the only source of NEW genetic variation.
Random with respect to fitness — don't preferentially generate beneficial alleles.
Most mutations are neutral or slightly deleterious; beneficials are rare.
Eukaryote rate ~10⁻⁸-10⁻⁹ per base/generation; dozens of new mutations per individual.

Mutation=heritable DNA change: point, indel, dup, inv, translocation·Mutation rate=~10⁻⁸-10⁻⁹ per base/gen in mammals·Random wrt fitness=mutation doesn't 'know' what's useful

L04 · Hardy-Weinberg Equilibrium

§A Allele freq vs genotype freq

For biallelic locus A,a: p = freq(A), q = freq(a). p + q = 1.
p = (2·N_AA + N_Aa)/(2·N_total).
Genotype freqs sum: freq(AA)+freq(Aa)+freq(aa) = 1.

Allele frequency=proportion of gene copies at a locus·Genotype frequency=proportion of individuals with a given genotype

§B The Hardy-Weinberg equation

HWE: p² + 2pq + q² = 1.
p² = AA freq; 2pq = Aa freq; q² = aa freq.
Five assumptions: no mutation, no migration, no drift, no selection, random mating.
HWE achieved in ONE gen of random mating from any starting genotype freqs.

HWE=allele/genotype freq constant; no evol forces acting·Random mating (panmixia)=all pairings equally likely

§C Detecting deviations

Excess homozygotes → inbreeding or population subdivision (Wahlund).
Excess heterozygotes → heterozygote advantage or disassortative mating.
Selection against a homozygote shifts allele freqs and genotype ratios.
Drift in small N causes random, non-directional departures.

Inbreeding=mating with relatives; raises homozygosity·Heterozygote advantage=Aa fitter than AA or aa (sickle/malaria)·Wahlund effect=apparent homozygote excess from pooling subpops

§D Worked computation pattern

Step 1: count alleles (AA→2A, Aa→1A+1a, aa→2a).
Step 2: compute p and q from totals.
Step 3: expected counts = N·p², N·2pq, N·q².
Step 4: compare expected vs observed; identify mechanism for mismatch.

Common slip: forgetting to multiply expected freqs by N when comparing to counts·Allele freqs alone can't detect HWE deviations — need genotypes

L05 · Quantitative Genetics, Selection, Plasticity

§A Variance partitioning

V_P = V_A + V_D + V_I + V_E.
V_A = additive (responds predictably to selection).
V_D = dominance (allele×allele same locus).
V_I = epistasis (allele×allele different loci).
V_E = environmental (not heritable).

V_A=additive genetic variance; passes parent→offspring; engine of selection·V_D=dominance variance; same-locus interactions·V_I=epistatic variance; cross-locus interactions·V_E=environmental variance; not inherited

§B Heritability — broad vs narrow

Broad-sense H² = V_G/V_P (V_G = V_A+V_D+V_I).
Narrow-sense h² = V_A/V_P — predicts response to selection.
h² estimated from parent-offspring regression (slope of offspring on mid-parent).
h² is population- and environment-specific; not intrinsic to the trait.

H²=V_G/V_P, total genetic over phenotypic variance·h²=V_A/V_P, narrow-sense; predicts evolution·Parent-offspring regression=offspring vs midparent slope ≈ h²

§C Breeder's equation

R = h² · S — central equation of quantitative genetics.
S = mean of breeders − population mean (selection strength).
R = mean of next gen − current mean (evolutionary response).
If h² = 0, R = 0 — no evolution regardless of selection strength.

S=phenotypic difference between breeders and population mean·R=change in pop mean from one gen to the next·Breeder's equation=R = h²·S

§D Phenotypic plasticity, reaction norms

Plasticity = one genotype produces different phenotypes in different environments.
Polyphenic = single genotype, discrete alternative morphs (winged/wingless aphids).
Reaction norm = phenotype-vs-environment plot for a genotype; sloped = plastic.
G×E = genotypes differ in HOW they respond (non-parallel reaction norms).

Phenotypic plasticity=one genotype, many phenotypes by environment·Reaction norm=phenotype vs environment plot·G×E=non-parallel reaction norms·Canalization=lack of plasticity

§E Selection vs evolution

Selection produces evolution ONLY when trait has heritable variation (h² > 0).
If V_A = 0, no evolutionary response no matter how strong selection.
Selection = within-gen process; evolution = between-gen outcome.

If trait differences are entirely environmental, R = h²·S = 0·Selection on phenotypes only matters if phenotypes correlate with genotypes

L07 · Empirical Studies of Natural Selection

§A Measuring selection in nature

Need (1) heritable variation, (2) differential reproduction, (3) freq change across gens.
Field requires longitudinal data — marked individuals tracked across years.
S measured directly: mean of breeders − population mean.
Predicted R = h²·S checked against next-gen change.

Selection in the wild=heritable trait variants reproduce more in nature

§B Grants' Galápagos finches

1977 drought left large hard seeds; deeper-beaked Geospiza fortis survived better.
Beak depth was heritable; next gen had measurably deeper beaks.
Wet years reversed the pressure (small seeds favored) — direction is contingent.
Hybridization with relatives also injected variation, mixing flow with selection.

Geospiza fortis=medium ground finch on Daphne Major·Selection on beak depth=post-1977 deeper beaks survived; next gen deeper

§C Peppered moths — industrial melanism

Pre-industrial: light morph dominant on lichen-covered trunks.
Pollution killed lichen, blackened trunks; melanic morph rose to >95% in polluted areas.
Mechanism: differential bird predation on visible morphs.
Clean-air laws → lichen returned → light morph rebounded.
Genetic basis: transposon insertion in cortex gene.

Industrial melanism=rise of dark morphs from human darkening·Biston betularia=peppered moth species

§D Other examples — flu, antibiotics, domestication

Influenza evolves antigenic variation under host immune + antiviral selection.
Antibiotic resistance — strong directional natural selection by humans.
Domestication = artificial selection; greyhounds show measurable evolution of speed.
Common structure: heritable variation + strong directional selection → rapid change.

Antibiotic resistance=resistant variants exist, drug selects them·Artificial selection=humans choose breeders

L08 · Complex Adaptations

§A Adaptation as trait and process

Adaptation (noun) = trait shaped by past selection; (verb) = the process producing it.
Complex adaptations build incrementally — many small mutational steps, each useful.
Each intermediate must itself be functional; selection cannot plan ahead.

Adaptation=trait shaped by past selection OR the process making it·Gradual evolution=complex traits via many small favorable changes

§B Vertebrate eye — stepwise model

Stage 1: light-sensitive patch (light/dark, circadian, predator detection).
Stage 2: cupped patch — directional sensitivity.
Stage 3: pinhole eye (Nautilus) — crude image, no lens.
Stage 4: lens added (co-opted crystallins) for sharp focus.
Eyes evolved independently >40 times — convergent solutions.

Stepwise eye evolution=patch→cup→pinhole→lensed, each stage functional·Convergent eye evolution=vertebrate vs cephalopod camera eyes

§C Regulatory networks, gene duplication

Cis-regulatory mutations alter when/where a gene fires without changing protein.
Gene duplication: one copy keeps original function; the other can evolve a new role.
Neofunctionalization vs subfunctionalization (split ancestral function).
Protein promiscuity — weak side activities can be refined into new primary functions.

Cis-regulatory mutation=enhancer/promoter change; alters expression·Gene duplication=extra copy; relaxed selection enables novelty·Neofunctionalization=duplicate gains new function·Subfunctionalization=duplicates split ancestral function·Protein promiscuity=weak side activities co-opted

§D Heterochrony

Heterochrony = evolution of timing/rate of developmental events.
Paedomorphosis: juvenile features kept in adult (axolotl).
Peramorphosis: development extended past ancestor (large antlers).
Small timing changes → dramatic morphological differences; simple genetic basis.

Heterochrony=evolution of developmental timing or rate·Paedomorphosis=juvenile features in adult (axolotl)·Peramorphosis=development extends past ancestral endpoint

§E Hox genes and conserved networks

Hox genes pattern A-P axis of bilaterians; arranged in clusters showing colinearity.
Same Hox toolkit patterns flies, mice, humans — deep conservation.
Body-plan differences come largely from changes in regulation, not Hox proteins.
Hox-cluster duplications correlate with major body-plan transitions (vertebrates have 4).

Hox gene=TF patterning A-P axis in bilaterians·Colinearity=Hox chromosomal order matches body-axis expression·Conservation of dev networks=Hox/Pax/Wnt shared across phyla

§F Imperfect adaptation

Selection produces 'good enough,' not optimal; constrained by history.
Vestigial structures (whale pelvis, human appendix) — ancestral function gone.
Trade-offs (running speed vs heat dissipation) limit any single trait.
Vertebrate retina has photoreceptors backwards — historical accident.

Vestigial structure=ancestral form, lost function·Trade-off=gain in one trait costs another·Constraint=historical/dev factor limiting selection

L09 · Coevolution

§A Defining reciprocal coevolution

Coevolution = reciprocal evolutionary change in interacting lineages.
Coexistence alone is NOT coevolution — adaptation must run in both directions.
Can be antagonistic (predator-prey) or mutualistic (pollinator-flower).

Coevolution=reciprocal evolutionary change between interacting species·Reciprocal selection=A imposes selection on B which imposes back on A

§B Antagonistic arms races

Newts (Taricha) make tetrodotoxin; garter snakes (Thamnophis) evolve TTX-resistant Na channels.
Geographic variation: where snakes are resistant, newts are toxic — and vice versa.
Arms races can be asymmetric; one side may temporarily 'win.'
Fitness costs (snake speed cost of resistance) cap escalation.

Coevolutionary arms race=reciprocal escalation of offense/defense·Tetrodotoxin (TTX)=newt neurotoxin blocking Na channels

§C Mutualistic coevolution

Pollinator-plant: long-tongued moths and long-spurred orchids (Darwin's prediction).
Endosymbiosis: mitochondria from alphaproteobacteria, chloroplasts from cyanobacteria.
Mutualisms can break down or shift to parasitism if cost/benefit changes.

Mutualism=both species gain net fitness·Endosymbiosis=organism inside another; origin of mitochondria/plastids

§D Mimicry — Batesian vs Müllerian

Batesian: harmless mimic resembles harmful model; mimic must stay rare.
Müllerian: multiple harmful species converge on shared warning signal.
Both products of frequency-dependent predator selection.

Batesian mimicry=palatable mimics unpalatable model·Müllerian mimicry=multiple unpalatable species share warning signal·Aposematism=warning coloration in unpalatable species

§E Geographic Mosaic Theory

Thompson: hotspots (intense reciprocal selection) + coldspots (weak/none).
Gene flow + local trait evolution → mosaic of coevolutionary states.
Predicts trait MISMATCH in some areas — evidence FOR ongoing coevolution.

Geographic Mosaic Theory=Thompson; coevolution varies in rate/direction across range

L11 · Sex and Sexual Selection

§A Cost of sex / why sex evolved

Twofold cost (Maynard Smith): sexual mom passes only half her genes per offspring.
Benefit 1: recombination shuffles alleles, makes new combinations selection can use.
Benefit 2: Muller's ratchet — sex purges deleterious mutations asexuals can't.
Benefit 3: Red Queen — sex helps hosts keep up with rapidly evolving parasites.
Benefit 4: sib competition reduced when offspring are diverse.

Twofold cost of sex=sexual female transmits half the gene copies of asexual·Muller's ratchet=asexual lineages accumulate irreversible mutations·Red Queen=sex needed to keep up with parasites

§B Anisogamy

Anisogamy = unequal gamete sizes; foundation of male/female.
Female = larger gamete sex; male = smaller. Defined by gametes, not behavior.
Asymmetric investment → asymmetric strategies (selective females, competitive males).

Anisogamy=unequal gametes; biological basis of sex·Isogamy=equal gametes (some algae/fungi); ancestral state

§C Sexual selection

Selection on traits raising MATING success rather than survival.
Intrasexual = same-sex contests (weapons, large body); intersexual = mate choice (ornaments).
Can OPPOSE survival selection — peacock tail attracts mates AND predators.
Fisherian runaway: arbitrary preference amplifies if 'sexy' offspring inherit both.

Sexual selection=selection for mating success rather than survival·Intrasexual=male-male combat·Intersexual=mate choice·Sexual dimorphism=morphological difference between sexes

§D Conflict, sperm competition

Sexual conflict: males benefit from many matings; females from fewer-but-better.
Sperm competition drives large testes, long sperm, mating plugs.
Cryptic female choice — bias paternity post-copulation via reproductive tract.
Antagonistic coevolution within species: males coerce, females resist (ducks, bedbugs).

Sexual conflict=opposing selection on males vs females·Sperm competition=sperm of different males compete to fertilize·Cryptic female choice=post-copulatory paternity bias·Antagonistic coevolution=reciprocal change from conflicting interests

L12 · Life History Evolution

§A Trade-offs in energy allocation

Growth vs reproduction; current vs future; offspring number vs size.
Trade-offs are physiological — selection navigates them, can't break them.
High adult survival favors future reproduction; low favors current.

Life history=schedule of birth/growth/reproduction/death·Trade-off=inverse relationship between fitness traits·Reproductive effort=fraction of resources allocated to current reproduction

§B Extrinsic mortality

HIGH extrinsic mortality → early reproduction, many offspring, short life.
LOW extrinsic mortality → delayed reproduction, fewer/better offspring, longer life.
Mainland (predators) opossums mature earlier than predator-free island opossums.
These shifts evolve in tens of generations under strong pressure.

Extrinsic mortality=external death (predation/disease)·Senescence/intrinsic mortality=physiological decline

§C Theories of senescence

Mutation accumulation (Medawar): late-life deleterious mutations escape selection.
Antagonistic pleiotropy (Williams): one gene helps young, hurts old — net favored.
Disposable soma (Kirkwood): trade-off between maintenance and reproduction.
Theories are not mutually exclusive — all may contribute.

Senescence=age-related decline in survival/reproduction·Mutation accumulation=many-gene story; late mutations escape selection·Antagonistic pleiotropy=single-gene story; early benefit, late cost·Disposable soma=invest in reproduction over repair

§D Age at maturity, offspring size

Earlier maturity → reproduce sooner but smaller; depends on growth/risk/payoff.
Many-small offspring (bet-hedging) vs few-large (well-provisioned, higher per-offspring).
r-selected: fast-living, many small (mice, weeds).
K-selected: slow-living, few large, parental care (elephants, oaks).

Age at maturity=age at first reproduction·r/K selection=fast-many vs slow-few life-history dichotomy

§E Seychelles warblers

Cooperative breeders: offspring help parents raise later broods.
Female offspring stay on natal high-quality territories; males disperse (sex-biased).
Helping is not pure altruism — helpers gain inclusive fitness, may inherit territory.

Cooperative breeding=adult helpers assist parents·Sex-biased dispersal=one sex disperses more than the other

L13 · Evolution of Social Behavior

§A Individual vs group selection

Naive group selection fails: cheaters profit without contributing, spread, collapse cooperation.
Modern view: selection mostly at individual or genic level; group benefits arise from individual.
Special conditions (frequent extinctions, strict subdivision) permit group selection but rare.

Group selection=differential reproduction of GROUPS·Selfish gene perspective=Dawkins; alleles favor their own propagation

§B Kin selection / inclusive fitness

Hamilton's rule: rB > C — altruism evolves when benefit×relatedness exceeds cost.
r values: parent-offspring 0.5; full sib 0.5; half sib 0.25; first cousin 0.125.
Inclusive fitness = direct (own offspring) + indirect (relatives' extra offspring × r).
Eusociality (bees, ants, naked mole-rats): workers forgo reproduction.
Haplodiploidy in hymenopterans: sisters r = 0.75 (more than to own offspring).

Hamilton's rule=rB > C; altruism favored when indirect benefit exceeds cost·Coefficient of relatedness (r)=prob of sharing allele by descent·Inclusive fitness=direct + indirect (kin-mediated)·Eusociality=reproductive division of labor; workers don't reproduce

§C Evolutionarily stable strategies (ESS)

ESS = strategy that, once common, can't be invaded by rare alternative (Nash equilibrium).
Depends on frequency-dependent payoffs.
Hawk-Dove: pure-Hawk unstable (costs); pure-Dove unstable (Hawks invade); mixed equilibrium.
ESS solved with payoff-matrix game theory.

ESS=strategy uninvadable when common·Frequency-dependent selection=fitness depends on strategy frequency·Hawk-Dove=classic ESS resource-competition game

§D Side-blotched lizards (rock-paper-scissors)

Three male morphs: Orange (aggressive), Blue (vigilant), Yellow (sneaker).
Orange > Blue, Blue > Yellow, Yellow > Orange — cyclic dominance.
Frequencies cycle over years; no single ESS, stable cyclic dynamic.
Real demonstration of negative frequency-dependent selection.

Side-blotched lizard (Uta stansburiana)=three throat-color morphs in RPS dynamics

§E Cooperation among non-kin

Direct reciprocity: tit-for-tat; needs repeat interaction and memory.
Indirect reciprocity: reputation attracts future help; needs visibility.
Mutualistic byproduct: cooperation costs nothing or directly benefits.
Cooperation among non-kin is fragile — needs enforcement to persist.

Direct reciprocity=tit-for-tat between two individuals·Indirect reciprocity=reputation-based; helping earns future help

L14 · History of Life

§A Earth's age, dating methods

Earth ~4.568 GYA (radiometric on meteorites, oldest zircons).
Radiometric: ratio of parent to daughter isotope; known half-life.
¹⁴C ~50 KYR limit; U-Pb for billions; K-Ar for millions.
Biomarkers (specific lipids) suggest life by ~3.5-3.8 GYA.

Radiometric dating=age from parent/daughter isotope ratios·Half-life=time for half a radioisotope to decay·Biomarker=lipid in old rock indicating organisms

§B Major milestones

~3.5-3.8 GYA: first life; ~2.4 GYA: Great Oxidation Event (cyanobacteria O₂).
~2.1-1.6 GYA: first eukaryotes (mitochondrial endosymbiosis).
~1.0 GYA: multicellularity; ~541 MYA: Cambrian explosion of phyla.
~252 MYA: end-Permian extinction (~95% marine sp lost).
~66 MYA: K-Pg / Chicxulub impact; non-avian dinosaurs gone.

Great Oxidation Event=O₂ rise ~2.4 GYA from cyanobacteria·Cambrian explosion=541-520 MYA rapid phylum diversification

§C Geological periods

Ordovician (~488-444 MYA): early bony fishes, first land plants.
Silurian (~444-416 MYA): first land animals (millipedes).
Devonian (~416-359 MYA): Age of Fishes; early tetrapods; forests.
Permian (~299-251 MYA): reptiles + synapsids; ends in biggest extinction.

Devonian=~416-359 MYA; fish diversification, first land vertebrates·Permian=~299-251 MYA; ends with largest mass extinction

§D Mass extinctions

Big Five: end-Ordovician, Late Devonian, end-Permian, end-Triassic, end-Cretaceous.
End-Permian (~252 MYA): largest; Siberian Trap volcanism + acidification + climate.
K-Pg (~66 MYA): Chicxulub asteroid; iridium layer is the smoking gun.
Survivors radiate into empty niches (mammals after K-Pg).
Many argue we're now in a sixth, human-driven extinction.

Mass extinction=geologically rapid >75% species loss·K-T (K-Pg) boundary=~66 MYA; non-avian dinosaurs gone·Iridium layer=K-Pg boundary marker; impact evidence

L15 · Phylogenetics and the Tree of Life

§A Reading phylogenetic trees

A node = common ancestor of taxa above it (toward tips).
Recency of common ancestor = closeness of relationship; not page distance.
Trees can be rotated at any node without changing relationships.

Tip/Terminal taxon=organism at branch end·Node=lineage divergence point; MRCA·Branch=lineage through time·Sister groups=clades sharing one immediate node

§B Synapomorphy / symplesiomorphy / homoplasy

Synapomorphy = shared derived character; defines monophyletic groups.
Symplesiomorphy = shared ancestral state; uninformative about closer relationships.
Homoplasy = independent acquisition or reversal; misleading.

Synapomorphy=shared derived state; informative for clade·Symplesiomorphy=shared ancestral state; uninformative·Homoplasy=convergent/parallel/reversed; not from common ancestor

§C Mono / para / polyphyletic

Monophyletic (clade) = ancestor + ALL descendants. The only valid group.
Paraphyletic = ancestor + some descendants (e.g., 'Reptilia' without birds).
Polyphyletic = members lacking shared immediate ancestor; built on convergence.

Clade/Monophyletic=ancestor + all descendants·Paraphyletic=ancestor + some descendants·Polyphyletic=group from convergent traits, no shared ancestor

§D Species concepts

Biological (Mayr): interbreeding populations reproductively isolated; fails for asexuals/fossils.
Morphological: distinct form; usable on fossils; cryptic species confuse it.
Phylogenetic: smallest monophyletic group with shared derived characters.

BSC=interbreeding populations, reproductively isolated·Morphological=diagnosable form differences·Phylogenetic=smallest monophyletic group

L16 · Species Concepts and Reproductive Isolation

§A Major species concepts

BSC (Mayr): interbreeding populations, reproductively isolated. Fails for asexuals/fossils.
Morphological: diagnosable differences; cryptic species and plasticity confuse.
Phylogenetic: smallest monophyletic group with shared derived chars.
Ecological: populations sharing one adaptive zone (niche).

BSC=interbreeding populations, reproductively isolated·Morphological=diagnosable form·Phylogenetic=smallest monophyletic group

§B Reproductive isolation

Prezygotic — temporal, behavioral, mechanical, gametic, habitat barriers.
Postzygotic — hybrid inviability, hybrid sterility (mules), hybrid breakdown (F2).
Dividing line is fertilization: pre = before zygote; post = after.

Prezygotic isolation=blocks fertilization (temporal/behavioral/mech/gametic/habitat)·Postzygotic isolation=blocks viable/fertile hybrids·Hybrid sterility=hybrids live but can't reproduce (mules)

§C Speciation modes

Allopatric: geographic separation → divergence → isolation. Most common in animals.
Peripatric: small founder population isolated; drift + selection accelerate divergence.
Parapatric: partially separated; divergence despite some gene flow.
Sympatric: divergence with no separation — niche shifts, polyploidy (mostly plants).
Reinforcement: secondary contact selects for stronger prezygotic isolation if hybrids unfit.

Allopatric=geographically separated populations·Sympatric=same range; niche shifts/polyploidy·Reinforcement=selection strengthens prezygotic isolation in secondary contact

§D Hybrid zones

Hybrid zones = regions of overlap and interbreeding between two species.
Viable hybrids typically have reduced fitness — outcompeted, sterile, or maladapted.
Zones can be stable (selection vs hybrids balanced by gene flow) or shift over time.
Hybrid speciation (sunflowers) is real but a special case.

Hybrid zone=geographic overlap with interbreeding·Viable hybrid=hybrid that survives but typically with reduced fitness

L17 · Biogeography, Speciation, Extinction

§A What is biogeography?

Biogeography = study of where species live and why.
Geological history (tectonics, glaciation) and ecology jointly shape distributions.
Wallace and Darwin: distinct continental faunas best explained by descent.

Biogeography=study of species distribution across space and time·Wallace line=Indonesian boundary between Asian and Australasian biotas

§B Dispersal vs. vicariance

Dispersal: organisms move; same lineage now in multiple regions.
Vicariance: a barrier (mountain, sea, drift) splits an existing range.
Often both operate; molecular dating distinguishes.
S. America-Africa biota relatedness reflects shared Gondwanan ancestry (vicariance).

Dispersal=organisms cross barriers·Vicariance=new barrier splits a continuous range

§C Standing diversity, turnover

Standing diversity = species count in a region at one time.
Turnover rate = species replacement over time.
Equilibrium island biogeography (MacArthur-Wilson): immigration vs. extinction balance.
Same standing diversity can mask very different turnover rates.

Standing diversity=species present at a moment·Turnover rate=species replacement per unit time

§D Mass extinctions

Big Five each killed >50% marine species; end-Permian (~252 MYA) is largest.
End-Permian: Siberian Traps + ocean acidification + climate; ~95% marine loss.
End-Triassic cleared major reptilian groups; dinosaurs dominated after.
K-Pg (~66 MYA): Chicxulub impact; iridium layer; mammals radiate.

Adaptive radiation=rapid diversification into many ecological niches

§E Adaptive radiations

Rapid diversification of one lineage into many niche-distinct species.
Conditions: open niches, new colonization, key innovations, post-extinction recovery.
Galápagos finches: ~14 species from one ancestor, each a food specialist.
Mammals radiated post-K-Pg as dinosaur niches opened.

Adaptive radiation=rapid lineage diversification across niches·Key innovation=novelty (jaws, wings, flowers) that opens new ecology

L18 · Conservation / Humans as Selective Force

§A Humans as selective force

Fisheries selection: size limits remove large individuals → earlier maturity, smaller size.
Trophy hunting (bighorn sheep): selecting big horns lowers average horn size.
Antibiotic use selects for resistant strains; pesticides for resistant insects.
Urbanization: city pigeons, mice, peppered moths evolve under novel pressures.

Selective harvest=hunting/fishing targeting specific phenotypes·Fisheries-induced evolution=size-selective fishing alters fish populations

§B Habitat fragmentation, conservation genetics

Small populations: strong drift, lost variation, inbreeding depression.
Fragmentation reduces gene flow, accelerates divergence and variation loss.
Florida panther: severe inbreeding (heart, reproductive issues); Texas puma rescue restored fitness.
Genetic rescue: introduce relatives to restore variation.

Inbreeding depression=fitness loss from homozygous deleterious recessives·Genetic rescue=introducing individuals to restore variation·Fragmentation=habitat subdivision; reduces gene flow

§C Climate change as selective pressure

Many species shifting ranges poleward and upslope.
Limited dispersers (trees, mountain-tops) face extinction or strong selection.
Phenological shifts: flowering, migration timing track climate.
Mismatches between interacting species can break ecological networks.

Phenological shift=timing change of seasonal events·Range shift=geographic move under warming, often poleward/upslope

§D Conservation strategies

Habitat protection (parks, reserves) — in-situ biodiversity.
Captive breeding (California condor, Arabian oryx) → reintroduction.
Assisted migration to climate-appropriate habitats; controversial.
Effective conservation manages BOTH demographic and genetic decline.

Conservation biology=preservation of biodiversity using evolutionary principles·Captive breeding=ex-situ to prevent extinction

L19 · Human Evolution

§A Hominin lineage and bipedalism

Hominins split from chimps ~6-7 MYA in Africa.
Earliest possible hominins: Sahelanthropus tchadensis (~7 MYA, Chad), Orrorin, Ardipithecus.
Bipedalism was the FIRST major hominin trait — preceded brain enlargement.
Foramen magnum positioned underneath the skull = upright spine.

Hominin=human lineage since chimp split·Bipedalism=habitual two-legged walking; first hominin hallmark·Foramen magnum=skull opening for spinal cord; position indicates posture

§B Australopithecines and early Homo

Australopithecus afarensis (~3.9-2.9 MYA): 'Lucy'; fully bipedal, small brain.
Robust australopithecines (Paranthropus): heavy chewing apparatus; dead-end.
Homo habilis (~2.5 MYA): genus Homo begins; first stone tools (Oldowan).
Homo erectus (~1.9 MYA): FIRST hominin to leave Africa; larger brain.
Homo sapiens emerges in Africa ~300 KYA.

Australopithecus=bipedal hominin ~4-2 MYA; Lucy = A. afarensis·Homo habilis=earliest Homo ~2.5 MYA; first stone tools

§C Out-of-Africa, Neanderthal/Denisovan

Modern Homo sapiens: ~300 KYA in Africa; major dispersal ~70 KYA.
Non-African humans: ~1-4% Neanderthal DNA (interbreeding ~40-60 KYA).
Asian/Oceanic populations carry Denisovan DNA; Tibetan EPAS1 high-altitude allele.
Introgression contributed alleles for immunity, pigmentation, altitude adaptation.

Out of Africa=Homo sapiens dispersal ~70 KYA·Introgression=gene flow via interbreeding between populations/species·Neanderthal=H. neanderthalensis; Europe/W. Asia; interbred ~40-60 KYA

§D Evolutionary medicine

Antibiotic resistance: pathogens evolve under drug selection; needs stewardship.
Virulence evolves with transmission mode: respiratory → low; vector-borne → high.
Mismatch hypothesis: ancestral (scarce, active) vs modern (abundant, sedentary) → obesity, T2D.
Body shows compromises: backaches, difficult childbirth, vestigial appendix.

Evolutionary medicine=evolutionary principles applied to health·Virulence=damage pathogen does to host·Mismatch hypothesis=modern disease from ancestral-modern environment gap

L20 · Evolutionary Medicine

§A What evolutionary medicine is

Asks WHY (evolutionary) bodies are vulnerable, not just HOW (mechanism).
Six explanations: mismatch, coevolution, constraints, trade-offs, reproduction trumps health, defenses confused as symptoms.
Modern medicine integrates: stewardship, vaccine design, cancer-treatment timing.

Evolutionary medicine=evolutionary biology applied to disease·Proximate vs ultimate=mechanism (HOW) vs evolutionary reason (WHY)

§B Pathogen evolution / antibiotic resistance

Resistance mutations occur randomly; antibiotics select pre-existing variants.
HGT spreads resistance genes between species via plasmids/transposons.
Mechanisms: enzymatic destruction, efflux pumps, target mods, alternative pathways.
Combination therapy: 10⁻⁹ × 10⁻⁹ = 10⁻¹⁸ for joint resistance — exponentially less likely.
Vaccine escape via antigenic drift (annual flu).

Antibiotic resistance=heritable bacterial drug survival from random mutation·HGT=DNA movement between species; speeds resistance spread·Combination therapy=multiple drugs needing multiple mutations·Antigenic drift=surface antigens evolve to evade immunity

§C Virulence and transmission mode

Virulence-transmission trade-off: load helps spread but kills hosts.
Directly transmitted (respiratory, STI) → moderate/lower virulence (need mobile hosts).
Vector-borne / waterborne (cholera, malaria) → high virulence (host mobility doesn't matter).
Ewald: cleaner water selects for less-virulent diarrheal pathogens.
1918 flu evolved high virulence under WWI crowding.

Virulence=host damage from pathogen·Virulence-transmission trade-off=load vs host longevity·Vector-borne=transmitted by third organism·Ewald's hypothesis=transmission mode shapes optimal virulence

§D Host-pathogen coevolution

Reciprocal: hosts evolve defense; pathogens evolve evasion; on and on.
MHC: highly variable; balancing selection from coevolving pathogens (rare alleles favored).
Red Queen at population level: sex evolved partly to keep up with parasites.
Sickle-cell allele persists via heterozygote advantage against malaria.

MHC=polymorphic immune genes presenting peptides; balancing selection·Sickle-cell heterozygote advantage=HbA/HbS protected from malaria·Antigenic variation=surface antigen evolution evading immunity

§E Mismatch hypothesis

Ancestral: food scarce, high activity, high pathogens, modest lifespan.
Modern: food abundant (refined sugars/fats), sedentary, hygienic, longer lifespan.
Efficient fat storage and sweet preference adaptive ancestrally → obesity now.
Hygiene hypothesis: low early-life microbe exposure → allergies, autoimmune.
Diseases of old age (most cancers, Alzheimer's) escape selection — post-reproductive.

Mismatch hypothesis=ancestral-modern environment gap drives modern disease·Hygiene hypothesis=low microbe exposure raises allergies/autoimmune·Diseases of civilization=chronic ills frequent only in modern populations

§F Cancer as somatic evolution

Tumor cells divide fast with high mutation rate — heritable variation among cells.
Cells compete for resources; growth-promoting mutations win.
Therapies are strong selection — kill susceptibles, leave resistant subclones → relapse.
Adaptive therapy: maintain susceptibles to suppress resistant subclones.
Cancer protection (apoptosis, senescence) trades off against regeneration/longevity.

Somatic evolution=mutation+selection on cell lineages within an organism·Tumor heterogeneity=genetic diversity among tumor cells·Adaptive therapy=keep susceptibles to suppress resistant clones