Chapter 13

How Populations Evolve

Campbell Biology: Concepts & Connections, 10th Global Ed.
Study Notes — Slides + Book Supplements

Legend: Plain text = from slides. FROM BOOK / [Book] = extra detail found only in the textbook, not
on the slides.
Contents
Contents .....................................................................................................................................2
Part I — Darwin’s Theory of Evolution .........................................................................................3
13.1 A Sea Voyage Helped Darwin Frame His Theory of Evolution ........................................3
13.2 The Study of Fossils Provides Strong Evidence for Evolution .........................................4
13.3 Scientific Thinking: Fossils of Transitional Forms Support Darwin’s Theory ....................4
13.4 Homologies Provide Strong Evidence for Evolution ........................................................5
13.5 Homologies Indicate Patterns of Descent Shown on an Evolutionary Tree .....................6
13.6 Darwin Proposed Natural Selection as the Mechanism of Evolution ...............................6
13.7 Scientists Can Observe Natural Selection in Action ........................................................7
Part II — The Evolution of Populations ........................................................................................8
13.8 Mutation and Sexual Reproduction Produce the Genetic Variation That Makes Evolution
Possible...................................................................................................................................8
13.9 Evolution Occurs Within Populations ..............................................................................8
13.10 The Hardy-Weinberg Equation Can Test Whether a Population Is Evolving .................9
13.11 Connection: The Hardy-Weinberg Equation Is Useful in Public Health Science ..........10
Part III — Mechanisms of Microevolution ..................................................................................11
13.12 Natural Selection, Genetic Drift, and Gene Flow Can Cause Microevolution...............11
13.13 Natural Selection Is the Only Mechanism That Consistently Leads to Adaptive
Evolution ...............................................................................................................................11
13.14 Visualizing the Concept: Natural Selection Can Alter Variation in Three Ways ...........12
13.15 Sexual Selection May Lead to Phenotypic Differences Between Males and Females .12
13.16 Evolution Connection: Drug-Resistant Microorganisms Are a Serious Public Health
Concern.................................................................................................................................13
13.17 Diploidy and Balancing Selection Preserve Genetic Variation .....................................13
13.18 Natural Selection Cannot Fashion Perfect Organisms ................................................14
Exam Quick-Reference .............................................................................................................15
Part I — Darwin’s Theory of Evolution
Three big ideas of the chapter: (1) Darwin’s Theory of Evolution, (2) The Evolution of
Populations, and (3) Mechanisms of Microevolution.
The theory of evolution is the idea that living species are descendants of ancestral species
that were different from present-day ones. It explains the diversity of life (>1.8 million species
identified, several million more estimated). Evolution is also happening right now, and the
environment plays a powerful role in it.

13.1 A Sea Voyage Helped Darwin Frame His Theory of Evolution

In simple terms: Darwin sailed around the world, saw tons of species that fit their environments,
and concluded life wasn’t created fixed and unchanging — species change over time and all share
common ancestors. He named this “descent with modification.”
• Charles Darwin is best known for On the Origin of Species by Means of Natural Selection
(“The Origin of Species”), which launched the era of evolutionary biology.
• His theory differed greatly from the long-held notion of a young Earth inhabited by
unchanging species.
• Darwin called his theory descent with modification, which explains that:
◦ all of life is connected by common ancestry, and
◦ descendants have accumulated adaptations to changing environments over vast
spans of time.
• Scientists regard evolution by natural selection as a theory — a widely accepted
explanatory idea that is broader in scope than a hypothesis, generates new hypotheses,
and is supported by a large body of evidence.
Checkpoint: What was Darwin’s phrase for evolution? → “Descent with modification” — an
ancestral species could diversify into many descendant species by accumulating adaptations to
various environments.
Figure 13.1A: The voyage of HMS Beagle (1831–1836).
FROM BOOK
Cultural/scientific context: Most scientists accepted Aristotle’s view that species are fixed,
permanent forms. Judeo-Christian culture reinforced this with a literal reading of Genesis; in the
1600s religious scholars estimated Earth’s age at only ~6,000 years.
Darwin’s background: As a boy he loved nature, fishing, hunting, and collecting insects. His
father sent him to medical school (he found it boring and surgery — before anesthesia —
horrifying, so he quit), then to Cambridge to become a clergyman. At age 22 he set sail on the
Beagle, a survey ship charting the South American coast for five years.
Key observations: Geographic proximity predicted relationships better than similarity of
environment — temperate South American species resembled tropical South American species
more than temperate European ones. He found a fossil armadillo “the size of a Volkswagen
Beetle.”
Galápagos: young volcanic islands ~900 km off South America. Most animals are found
nowhere else but resemble mainland species (e.g., marine iguanas with a flattened, swimming
tail; each island had its own giant tortoise — galápago = “tortoise” in Spanish).
Influence of Charles Lyell’s Principles of Geology: an ancient Earth shaped over millions of
years by slow geologic processes that still operate. After witnessing a Chilean earthquake raise
the coast, Darwin reasoned marine fossils high in the Andes were lifted by such forces.
Wallace & publication: In 1858 Alfred Russel Wallace independently conceived a nearly
identical hypothesis; facing the risk of being scooped, Darwin released his essay, and published
The Origin of Species in 1859. Its predictions have been tested and verified by 150+ years of
research. Modern definition of evolution extends Darwin’s phrase to “genetic changes in a
population from generation to generation.”

13.2 The Study of Fossils Provides Strong Evidence for Evolution

In simple terms: Fossils are old remains/imprints buried in rock layers. Because deeper layers are
older, fossils show that life has changed over time and that many species died out — direct evidence
that evolution happened.
• Fossils are the imprints or remains of organisms that lived in the past; they document
differences between past and present organisms and reveal that many species have
become extinct.
• The fossil record reveals the historical sequence in which organisms have evolved.
Slide examples: Skull of Homo erectus; ammonite casts; strata of sedimentary rock at Gozo
Island, Malta.
FROM BOOK
How fossils form: Soft organic matter usually decays fast, but mineral-rich hard parts (bones,
teeth, shells) may remain. Some fossils are not actual remains — e.g., 375-million-year-old
ammonite casts form when a buried organism decays, leaving a mold later filled by dissolved
minerals that harden into a replica. Imprints, footprints, burrows, and fossilized feces (coprolites)
record behavior.
Rare whole-body preservation: insects in amber (fossilized tree resin); mammoths, bison, and
prehistoric humans frozen in ice or preserved in bogs.
Strata (singular stratum): layers of sedimentary rock. Younger strata sit on older ones, so
relative fossil age is read from the layer. The Homo erectus skull is ~1.5 million years old;
Gozo’s exposed layers formed in the Tertiary, ~30–35 million years ago.
Checkpoint: Which organisms are least represented in the fossil record? → Those lacking hard
parts (e.g., jellyfish, mushrooms) and those living where sedimentary rock did not form.

13.3 Scientific Thinking: Fossils of Transitional Forms Support Darwin’s

Theory
In simple terms: Whales evolved from land mammals. A chain of fossils (Pakicetus → … → modern
whale) shows legs gradually shrinking into flippers — a step-by-step “in between” record exactly like
Darwin predicted.
• Many fossils link early extinct species with species living today; thousands of discoveries
illuminate the evolutionary origins of many groups.
• Beginning in the late 1970s, paleontologists unearthed transitional fossils and thought
whales arose from a wolf-like carnivore.
• Molecular biologists found a close relationship between whales and hippopotamuses,
hypothesizing both descended from a cloven-hoofed ancestor.
• Two fossils discovered in 2001 resolved it: both Pakicetus and Rodhocetus had the
distinctive ankle bone of a cloven-hoofed mammal — so confidence in the whale origin
grew as different lines of evidence converged.
Figure 13.3: Progressive reduction of hind-limb and pelvic bones across Pakicetus →
Ambulocetus → Rodhocetus → Dorudon → modern cetacean (humpback). Key colors: pelvis,
femur, tibia, foot.
FROM BOOK
Darwin predicted transitional fossils linking very different groups. Whales are cetaceans (with
dolphins and porpoises): forelimbs are flippers, hind limbs absent — so transitional forms should
show reduced hind limb and pelvic bones.
Series details: Pakicetus (~50 Mya, “whale of Pakistan”) was a wolf-sized carnivore with land-
animal limbs but cetacean middle-ear structures. Ambulocetus (~48 Mya, “walking whale”) had
land-mobile forelimb joints plus a powerful tail and paddle-like hind feet. Rodhocetus (~46 Mya)
had short limbs and long-toed webbed feet. Dorudon (40–35 Mya) was fully aquatic — paddle
forelimbs couldn’t walk, hind limbs tiny, pelvis not connected to the vertebral column.
Other documented transitions: fish→amphibian, origin of birds from dinosaurs, mammals from a
reptilian ancestor. A cloven hoof is a hoof split into two toes; hippos belong to a group with pigs,
deer, and camels.
Checkpoint: What feature did scientists predict in transitional terrestrial→aquatic mammals? →
Reduced hind limb and pelvic bones.

13.4 Homologies Provide Strong Evidence for Evolution

In simple terms: Different animals share the same underlying parts (e.g., the same arm bones in a
human, cat, whale, and bat) even when they’re used differently. Same blueprint = inherited from a
shared ancestor. Leftover useless parts (vestigial structures) are clues too.
• Evolution is descent with modification — a remodeling process. Related species can share
underlying structural similarity yet function differently.
• Homology = similarity resulting from common ancestry. Structural and molecular
homologies reveal evolutionary relationships.
• Homology explains why early developmental stages of different animals share similarities
not visible in adults.
• Vestigial structures are remnants of features that served important functions in the
organism’s ancestors.
Slide figures: Homologous vertebrate forelimbs (human, cat, whale, bat — same
humerus/radius/ulna/carpals/metacarpals/phalanges); homologous structures in vertebrate
embryos (pharyngeal pouches and post-anal tail in chick and human embryos).
FROM BOOK
Homologous structures = features that often have different functions but are structurally
similar because of common ancestry (e.g., a whale’s flipper vs. a bat’s wing are variations on
one ancestral limb). If they had been uniquely engineered, their basic designs would differ.
Molecular homology: all life uses the same DNA/RNA language and an essentially universal
genetic code — evidence that all species descend from common ancestors. Closely matching
homologous gene sequences imply a recent common ancestor; more sequence differences
imply a more distant one. (This is why bacteria engineered with human genes can make insulin
or growth hormone.)
Embryos: at some point all vertebrate embryos have a post-anal tail and pharyngeal (throat)
pouches; the pouches develop into gills in fishes and into ear/throat parts in humans.
Pseudogenes: inactivated genes that have lost function while homologs in related species stay
functional. Example — humans and other primates carry the inactive GLO gene (an enzyme for
making vitamin C), so we must get vitamin C from diet. Vestigial example: tiny pelvis/hind-leg
bones of ancient whales; reduced eye remnants under scales in blind cave fishes.
Checkpoint: “Insect and bird wings are not homologous” means the wings evolved
independently from different original structures (analogous, not inherited from a common winged
ancestor).

13.5 Homologies Indicate Patterns of Descent Shown on an Evolutionary Tree

In simple terms: An evolutionary tree is a family tree for species. Each branch point is a shared
ancestor; the closer two species branch, the more recently they split. Shared traits tell you who’s
related to whom.
• Biologists represent patterns of descent with an evolutionary tree, often drawn sideways.
• Homologous structures — anatomical and/or molecular — determine the branching
sequence of the tree.
Reading Figure 13.5 (tetrapods + lungfishes): Each branch point = the common ancestor of
the lineages to its right. A purple hatch mark = a homologous (shared, derived) character
shared by all groups to its right. Shown: tetrapod limbs (ancestor 2), amnion (ancestor 3),
feathers (ancestor 6).
FROM BOOK
Darwin was the first to picture the history of life as a branching tree. Some homologies (e.g., the
genetic code) are shared by all species because they are very ancient; characters that evolved
more recently are shared only within smaller groups.
Worked relationships: lungfishes + all tetrapods descend from ancestor 1; crocodiles + birds
descend from ancestor 5. Tetrapod limbs (ancestor 2) appear in all its descendants; the amnion
(ancestor 3) is shared only by mammals and reptiles; feathers (ancestor 6) only in birds.
Evolutionary trees are hypotheses; some are strongly supported by combined fossil, anatomical,
and molecular data, while others are more speculative when data are scarce.
Checkpoint: Are amphibians more closely related to lungfishes or mammals? → Mammals —
amphibians and mammals share a more recent common ancestor (2) than amphibians share
with lungfishes (1).

13.6 Darwin Proposed Natural Selection as the Mechanism of Evolution

In simple terms: Breeders reshape animals fast by choosing who reproduces (artificial selection).
Darwin said nature does the same thing slowly: the environment “chooses” survivors, and over many
generations populations change. Populations evolve, not individuals.
• Darwin’s greatest contribution was his explanation of HOW life evolves.
• Insight came from artificial selection — selective breeding of domesticated
plants/animals to promote desirable traits (e.g., fancy pigeons bred from the rock pigeon;
dog breeds from the gray wolf).
• Darwin reasoned: if artificial selection causes large change quickly, natural selection could
modify species considerably over hundreds or thousands of generations.
Three key points about natural selection:
1. Individuals do not evolve; populations evolve over time (selection acts through individual–
environment interactions, but the group changes).
2. Natural selection can amplify or diminish only heritable traits.
3. Evolution is not goal-directed; it does not produce perfectly adapted organisms.
FROM BOOK
Two components of artificial selection: variation (differences among individuals let breeders pick
stock) and heritability (transmission of a trait from parent to offspring). Examples of dramatic
change: tomatoes from blueberry-sized Peruvian ancestors; dachshunds from wolves.
Malthus’s influence: economist Thomas Malthus argued populations grow faster than resources.
Darwin applied this — overproduction of offspring → a struggle for existence with only some
surviving. The essence of natural selection is this unequal reproduction: individuals whose traits
better enable them to obtain food, escape predators, or tolerate conditions survive and
reproduce more, passing on adaptive traits.
Point 2 detail: acquired characteristics (e.g., a bodybuilder’s muscles) are not passed on unless
coded in gametes — “a championship female bodybuilder will not give birth to a muscle-bound
baby.” Point 3 detail: a trait favorable in one situation may be useless or harmful in another,
because the environment varies in place and time.
Checkpoint: Artificial vs. natural selection — in artificial selection humans choose desirable
traits and breed those organisms; in natural selection the environment does the choosing, and
the best-suited individuals reproduce most successfully.

13.7 Scientists Can Observe Natural Selection in Action

In simple terms: We can watch evolution happen now. Spray a pesticide and the few naturally-
resistant bugs survive and multiply, so the whole population becomes resistant. Selection doesn’t
create the resistance — it just filters for bugs that already had it.
• Biologists have documented evolutionary change in thousands of studies.
• Classic unsettling example: pesticide resistance in hundreds of insect species. A new
pesticide initially kills most insects, but genetically resistant survivors reproduce, so the
resistant proportion rises with each generation and later applications become less
effective.
Two important points (slides):
4. Natural selection is more an editing process than a creative mechanism — it does not
create new alleles.
5. Natural selection is contingent on time and place — it favors heritable traits that fit the
current, local environment.
FROM BOOK
Grants’ finch study: over 30+ years on the Galápagos, Peter and Rosemary Grant measured
ground-finch beak size. In dry years (few small seeds) larger, stronger beaks had an advantage
and average beak depth increased; in wet years smaller beaks were more efficient and average
beak depth decreased.
Pesticide mechanism detail: the few survivors carry a pre-existing resistance allele; the poison
does not create resistance, it selects for it. Related real example: over-the-counter head-lice
treatments now fail in many areas because of resistant “super lice.”
Checkpoint: Natural selection “edits” rather than creates — it cannot make beneficial alleles on
demand; it selects among variation already present for individuals best suited to the current
environment.
Part II — The Evolution of Populations

13.8 Mutation and Sexual Reproduction Produce the Genetic Variation That
Makes Evolution Possible
In simple terms: Evolution needs variety to work on. Mutations create brand-new gene versions (the
original source), and sex reshuffles existing genes every generation, so offspring are all slightly
different.
• Organisms typically show individual variation.
• Mutations are the ultimate source of the genetic variation that is the raw material for
evolution.
• In sexually reproducing organisms, most genetic variation comes from the unique
combination of alleles each individual inherits.
Three random components of sexual reproduction that create fresh allele assortments
each generation:
6. crossing over,
7. independent orientation of homologous chromosomes at metaphase I of meiosis, and
8. random fertilization.
FROM BOOK
Phenotype vs. genotype: only the genetic component of variation is heritable and relevant to
selection (e.g., straightened teeth from dental work aren’t passed on). Variation can be
polygenic (continuous, like human height) or controlled by a single locus (discrete, like blood
types).
Mutation detail: a mutation is a change in the nucleotide sequence of DNA; only mutations in
gamete-producing cells affect a population. Most mutations affecting protein function are
harmful, but a rare one can improve fit — especially when the environment changes (e.g., DDT-
resistance mutations in houseflies were a handicap before DDT but advantageous after).
Chromosomal mutations that delete/disrupt/rearrange loci are usually harmful, but gene
duplication provides important new raw material: duplicate copies can accumulate mutations
and evolve novel functions (e.g., mice have ~1,300 olfactory receptor genes from repeated
duplication).
Speed: in prokaryotes (haploid, fast-dividing) a beneficial mutation can spread in hours/days
and acts immediately. In animals/plants, mutation rates average ~1 in 100,000 genes per
generation; low rates, long generations, and diploidy keep generation-to-generation variation
low.
Checkpoint: Ultimate source of variation = mutation; source of most variation in a sexual
population = unique allele combinations from sexual reproduction.

13.9 Evolution Occurs Within Populations

In simple terms: Zoom out: evolution is measured as shifting allele frequencies in a whole
population’s gene pool over generations (microevolution). A single organism can’t evolve — only the
group does.
• A population = a group of individuals of the same species that live in the same area and
interbreed.
• A gene pool = all copies of every type of allele, at every locus, in all members of the
population.
 • Microevolution = a change in the frequencies of alleles in a population’s gene pool —
evolution on its smallest scale.
Slide figure: Lakes in Alaska / stickleback fish illustrate isolated populations (fully plated, low
plated, very low plated, naked).
FROM BOOK
Common misconception corrected: individual organisms do not evolve during their lifetimes.
Natural selection acts on individuals, but evolutionary impact appears only as changes across a
population over generations — an individual’s genetic makeup rarely changes in its lifetime.
Populations of one species can be geographically isolated (e.g., separate lakes or islands; each
Galápagos tortoise population is restricted to its island), so gene exchange is rare. Members of
a population are typically more closely related to each other than to members of another
population.
Example of microevolution: a mosquito population with two DDT-related alleles; in DDT-sprayed
fields the resistance allele rises and the other falls — a change in the gene pool over
generations.
Checkpoint: Why can’t an individual evolve? → Evolution is a change in a population’s genetic
makeup over time; an individual’s genetic makeup rarely changes during its life.

13.10 The Hardy-Weinberg Equation Can Test Whether a Population Is

Evolving
In simple terms: This is the “nothing-is-happening” baseline. If a population is large, mates
randomly, and has no mutation/migration/selection, allele frequencies stay frozen (p+q=1,
p²+2pq+q²=1). If real numbers drift away from this prediction, evolution is occurring.
• The Hardy-Weinberg equilibrium states that allele and genotype frequencies stay
constant if the population is large, mating is random, and there is no mutation, gene flow,
or natural selection.
• The equation can be used to test whether evolution is occurring in a population.
Worked example — imaginary iguanas (foot webbing; W dominant nonwebbed, w
recessive webbed):
Genotype WW Ww ww
Number (total 500) 320 160 20
Genotype frequency 0.64 0.32 0.04
Counting alleles (1,000 total): W = (2×320)+160 = 800 → p = 0.8; w = 160+(2×20) = 200 → q =
0.2. Note p + q = 1.
Next generation via Punnett square (gametes carry parental allele frequencies): WW = p² =
0.64, Ww = 2pq = 0.32, ww = q² = 0.04. Frequencies are unchanged → the population is in
Hardy-Weinberg equilibrium.
Equations: p + q = 1 and p² + 2pq + q² = 1 (p² = homozygous dominant, 2pq = heterozygotes,
q² = homozygous recessive).
FROM BOOK
Why the dominant allele does not “take over”: the shuffling of alleles in sexual reproduction does
not change allele frequencies — they stay constant unless an outside factor acts. Hardy and
Weinberg derived this independently in 1908.
Five conditions for HW equilibrium: (1) very large population, (2) no gene flow, (3) no
mutation, (4) random mating, (5) no natural selection. Because these are rarely all met, real
frequencies usually do change.
Checkpoint: Least likely to alter frequencies over a few generations in a large sexual
population? → Mutation, because mutations are rare, so their per-generation effect is small.

13.11 Connection: The Hardy-Weinberg Equation Is Useful in Public Health

Science
In simple terms: Doctors use the same math to estimate hidden carriers of recessive diseases.
Knowing how many people have a disease (q²) lets you calculate how many silently carry one copy
of the allele (2pq) — e.g., ~2% carry the PKU allele.
• Public health scientists use the equation to estimate how many people carry alleles for
inherited diseases.
• About 1 in 10,000 U.S. babies has phenylketonuria (PKU) — an inherited inability to
break down the amino acid phenylalanine.
• PKU health problems can be prevented by a diet that limits phenylalanine (hence
aspartame warning labels on foods).
FROM BOOK
Worked PKU calculation: PKU is recessive, so affected frequency = q² = 0.0001 → q = 0.01,
and p = 1 − q = 0.99. Carrier frequency = 2pq = 2 × 0.99 × 0.01 = 0.0198 → about 2% (1.98%)
of the U.S. population carry the PKU allele. Untreated PKU causes brain damage; newborns are
routinely screened.
Checkpoint: Which term gives the frequency of individuals with NO PKU alleles? → p².
Part III — Mechanisms of Microevolution

13.12 Natural Selection, Genetic Drift, and Gene Flow Can Cause
Microevolution
In simple terms: Three things change a gene pool: selection (best-fit survive), genetic drift (random
luck, big effect in small groups — bottleneck & founder effects), and gene flow (individuals moving
in/out). Only selection reliably improves fit; the others are mostly chance.
The three main causes of evolutionary change:
9. Natural selection,
10. Genetic drift, and
11. Gene flow.
• Two situations producing genetic drift:
◦ Bottleneck effect — loss of genetic diversity when a population is drastically
reduced.
◦ Founder effect — genetic drift when a few individuals colonize an island or new
habitat.
FROM BOOK
Genetic drift = chance fluctuations in allele frequencies; the smaller the population, the bigger
the effect (coin-flip analogy: 7/3 heads in 10 flips is normal; 700/300 in 1,000 is not). An allele
can be lost entirely from a small population.
Natural selection detail: the “no selection” condition is essentially never met — e.g., webbed-
foot (ww) iguanas might swim and feed better, raising the w allele frequency.
Bottleneck examples: greater prairie chicken (Illinois numbers crashed to ~50 by 1993, lowering
hatching success); African cheetah (two bottlenecks — Pleistocene extinction and hunting —
leaving <5% of needed genetic variability); Florida panther. Even after recovery, a bottlenecked
population may keep low genetic variation.
Founder effect example: Tristan da Cunha — in 1814, 15 colonists founded a settlement; one
carried a recessive retinitis pigmentosa allele, which by the 1960s was ~10× more frequent
there than in the source British population.

13.13 Natural Selection Is the Only Mechanism That Consistently Leads to

Adaptive Evolution
In simple terms: Drift and gene flow are random, so they only improve an organism’s fit by luck.
Natural selection is non-random, so it’s the one mechanism that consistently makes species better
matched to their environment. “Fittest” = most fertile offspring, not strongest.
• Only natural selection consistently produces adaptive evolution — a better fit between
organisms and their environment.
• Relative fitness = the contribution an individual makes to the next generation’s gene pool
relative to other individuals.
• As a result of natural selection, favorable traits increase in a population.
FROM BOOK
Why only selection: among microevolution causes, only the variation-producing events
(mutation, sexual reproduction) are random — the selection process itself (better-adapted
individuals reproduce more) is non-random, so it consistently improves fit. Drift, gene flow, and
mutation improve fit only by chance.
“Survival of the fittest” is misleading: fitness is usually subtle and reproductive, not direct
combat. The fittest are those that produce the most viable, fertile offspring. Example: the blue-
footed booby’s torpedo-shaped body, braking tail, and webbed-feet flippers suit diving and
fishing — but a “good match” is a moving target because environments change.
Checkpoint: “Survival of the fittest” vs. relative fitness — survival alone doesn’t guarantee
reproductive success; relative fitness is measured by number of fertile offspring contributed to
the next gene pool.

13.14 Visualizing the Concept: Natural Selection Can Alter Variation in Three
Ways
In simple terms: Selection can push a trait three ways: toward one extreme (directional), toward the
middle (stabilizing), or toward both extremes at once (disruptive). Think: shift the curve, narrow the
curve, or split the curve in two.
• Stabilizing selection — favors intermediate phenotypes (removes both extremes;
maintains the status quo).
• Directional selection — shifts the population by acting against individuals at one
phenotypic extreme.
• Disruptive selection — favors individuals at both ends of the range over intermediates
(when conditions vary).
Slide examples: directional = cliff swallows (larger bodies survived a cold snap); stabilizing =
human birth weight (~6–8 lb best; very small/large less likely to survive); disruptive = African
black-bellied finches (small or large beaks beat medium beaks).
FROM BOOK
Selection acts on the phenotype (physical traits, metabolism, behavior), which is what the
environment directly exposes. Directional selection is common when the environment changes
or members migrate to a new habitat; disruptive selection can produce two or more contrasting
forms in one population.
Checkpoint: Which type likely produced the color/banding variation in the brown-lipped snails
(Fig. 13.8)? → Disruptive selection.

13.15 Sexual Selection May Lead to Phenotypic Differences Between Males

and Females
In simple terms: Some traits exist just to win mates, not to survive better. Either males fight each
other (intrasexual) or one sex picks the flashiest partner (mate choice). Flashy features like a
peacock’s tail can signal “good genes,” so they spread even if risky.
• Sexual selection = a form of natural selection in which individuals with certain
characteristics are more likely to obtain mates.
• Secondary sex characteristics can give an individual a mating advantage (e.g., peacock
vs. peahen — extreme sexual dimorphism).
• Intrasexual selection — individuals compete directly with the same sex for mates (e.g.,
male elk contests).
• Intersexual selection (mate choice) — the more common type; one sex (usually
females) is choosy in selecting mates.
FROM BOOK
Sexual dimorphism = differences between sexes not directly tied to reproduction (size, manes,
plumage); males are usually the showier sex among vertebrates. Intrasexual selection often
appears where a winner gains a harem; contests are frequently ritualized displays rather than
combat.
Mate-choice paradox: showy traits (e.g., a peacock’s tail) can be costly/risky (more visible to
predators) yet are reinforced because they raise reproductive success. Choosing such a male
perpetuates both his alleles and the alleles for the female’s preference.
“Good genes” hypothesis: showy traits may signal health. In gray tree frogs, females prefer long
mating calls; offspring of long-callers grew bigger and faster and survived better than half-
siblings of short-callers — the call duration indicated overall genetic quality.
Checkpoint: Why is choosing an elaborately ornamented male advantageous? → The display
may signal good health/good genes that can be passed to her offspring.

13.16 Evolution Connection: Drug-Resistant Microorganisms Are a Serious

Public Health Concern
In simple terms: Antibiotics work like pesticides on bacteria: the resistant ones survive and take
over. Overusing antibiotics and stopping early speeds this up. The drugs don’t “create” resistance —
they select for resistant germs that were already there.
• Just as pesticides select for resistant insects, antibiotics select for resistant bacteria.
We worsen antibiotic resistance when:
12. doctors overprescribe antibiotics,
13. patients stop taking antibiotics too early, and
14. livestock producers add antibiotics to feed as growth promoters / to prevent illness.
• In 2013 the CDC reported drug-resistant microorganisms infect >2 million people and
cause 23,000 deaths per year in the U.S.; the CDC identified 15 microorganisms posing
urgent or serious threats.
FROM BOOK
Mechanism: a gene for an enzyme that breaks down an antibiotic, or a mutation altering the
antibiotic’s binding site, makes a bacterium and its offspring resistant — again random mutation
+ non-random selection. MRSA (methicillin-resistant Staphylococcus aureus) was an early
warning; staph spreads in hospitals and community settings and can be fatal in the
bloodstream.
Premature stopping lets slowly-killed mutant bacteria survive and multiply, opening the door to
full resistance. The same logic explains chloroquine resistance (and eventually artemisinin
resistance) in the malaria parasite. Before penicillin (1940s), minor wounds could be fatal.
Checkpoint: Why is “Antibiotics have created resistant bacteria” wrong? → Antibiotics did not
create new alleles; their use increased the frequency of resistance alleles already naturally
present in the population.

13.17 Diploidy and Balancing Selection Preserve Genetic Variation

In simple terms: Why doesn’t selection erase all variety? Two sets of chromosomes hide recessive
alleles in carriers, and sometimes carriers (heterozygotes) survive best — like sickle-cell carriers
resisting malaria — which keeps both alleles around.
• Diploidy preserves variation by “hiding” recessive alleles (protected from selection in
heterozygotes).
 • Balancing selection — natural selection maintains stable frequencies of two or more
phenotypic forms in a population.
• Heterozygote advantage — a type of balancing selection in which heterozygotes out-
reproduce both homozygotes, keeping two or more alleles in the population.
Slide figure: Map of sickle-cell allele frequency vs. malaria incidence in Africa/Asia.
FROM BOOK
Why variation isn’t eliminated: selection acts on phenotype, and recessive alleles only show in
homozygous recessives — in heterozygotes they are shielded, so a large hidden pool of alleles
persists that could be useful if the environment changes.
Sickle-cell example: heterozygotes are protected from the worst effects of malaria;
homozygous-normal individuals are selected against by malaria, and homozygous sickle-cell
individuals by sickle-cell disease. The sickle-cell allele is highest where malaria is a major cause
of death (e.g., West Africa). It first emerged ~10,000 years ago — not an ideal solution (even
heterozygotes can have problems), but adaptations are often compromises.
Checkpoint: Why does selection reduce variation more in haploid than diploid organisms? → In
haploids every allele is phenotypically expressed and thus directly screened by selection (no
heterozygous hiding).

13.18 Natural Selection Cannot Fashion Perfect Organisms

In simple terms: Evolution can’t build perfection. It only works with the variation available, is stuck
remodeling ancestral parts, makes trade-off compromises, and gets pushed around by chance. So
bodies are “good enough,” not ideal — and the flaws prove evolution happened.
Evolution is constrained for four reasons:
15. Selection can act only on existing variations — new advantageous alleles do not arise
on demand.
16. Evolution is limited by historical constraints — it co-opts and remodels existing structures
rather than building from scratch.
17. Adaptations are often compromises — one structure must serve many functions.
18. Chance, natural selection, and the environment interact — environments change
unpredictably.
FROM BOOK
Detail: e.g., birds and bats evolved flight from four-legged ancestors, leaving only two limbs for
walking (historical constraint). The blue-footed booby’s webbed feet are great for swimming but
clumsy on land (compromise). A storm may blow non-ideal insects to an island, and drift can
lose beneficial alleles in small populations (chance).
Bottom line: natural selection operates on a “better than” basis, not toward perfection — the
imperfections of organisms are themselves evidence of evolution.
Checkpoint: Why are humans prone to sprains and dislocations despite flexible joints? →
Adaptations are compromises — structural reinforcement was traded off as agility was selected
for.
Exam Quick-Reference
FROM BOOK
Darwin’s logic (observations → inferences): Overproduction of offspring + heritable variation
→ individuals well suited to the environment leave more offspring → over time, favorable traits
accumulate in the population.
Two key equations: p + q = 1; p² + 2pq + q² = 1.
Sample calc (review Q12): If sickle-cell disease (recessive) affects 1 in 50 (q² = 0.02), then q =
√0.02 ≈ 0.141, p ≈ 0.859, carriers 2pq ≈ 0.243 → ~24% are carriers.
Fitness (review Q4): Best measure of fitness = how many fertile offspring an organism
produces.
NOT an influence on Darwin (review Q3): Mendel’s paper on inheritance (its significance
wasn’t recognized until 1900, after Darwin).
HIV / 3TC resistance (review Q8): A few drug-resistant viruses were present at the start of
treatment; natural selection increased their frequency — the drug selected, it did not induce
resistance.
Lamarck vs. Darwin (review Q11): Lamarck proposed inheritance of acquired characteristics
(use/disuse, e.g., giraffe necks stretched longer). Modern genetics rejects this: acquired traits
aren’t passed on unless encoded in gametes; selection acts on heritable variation, not on traits
gained during a lifetime.