Notes: Chapters 3-8. This covers through the first exam

Chapter 3: Natural Selection (as presented in this chapter phenotypic selection)
• Artificial selection
• The syllogism of evolution by natural selection
• Galapagos Finches - an extended example
• Conceptions & misconceptions about evolution by selection

Artificial selection
Even in Darwin’s time, it was clear that by choosing some individuals over others to reproduce, one could cause a large
amount of change and diversification, far beyond the original range of variation
e.g. cabbage, broccoli, kale, kolrabi, brussel sprouts, cauliflower
breeds of dogs, pigeons, etc.

The syllogism of evolution by natural selection
1. Individuals within populations vary
2. Part of this variation is heritable (we now know caused by particulate alleles)
3. Some individuals are more successful at surviving and reproducing (are more ‘fit’) than others
4. Some of the variation in fitness is caused by the variation in traits
When these premises are true, there will be a change in the frequencies of the traits from generation to generation (assuming no complications)
We call this type of change ‘evolution’
(Micro)evolution is change in allele frequencies across generations

Fig. 3.4 Galapagos finches - notice diversity of beaks
1. Is there variation in beak dimensions in Geospiza fortis? Fig. 3.6. Yes.
2. Is some of this variation heritable? Fig. 3.7. Yes. Complications could include misidentified paternity, nest parasitism, maternal effects, shared environments, but the evidence from, extra-pair matings, argues against most of these.
3. Do individuals vary in fitness? Yes, only some survive and only some reproduce (Fig. 3.8a shows that a bunch of them died) ... which was related to the
abundance of seeds (3.8b)…and which ones died followed the size of the available food (3.8c)
4. Was fitness related to trait variation? Yes. Individuals with deeper beaks survived better than those with finer beaks during the drought (3.9)
So, they evolved (3.10)

Conceptions and misconceptions about evolution through selection
• Selection sorts among individuals, but the population is what evolves
• Selection acts on phenotypes, but evolution is a change in gene frequencies
• The adaptive process is not forward-looking; every step is a response to immediate conditions
• New states can evolve beyond what was previously present
• Correlated response to selection complicates optimization
• Selection is non-random (mutation is what is undirected)
• Evolution can be ‘up’ or ‘down’ and can change direction (there is no sense of uni-directional progress)
• Fitness is not tautological: the realities of physics etc. cause relationships between traits and fitness
• Selection acts among individuals, not usually for the good of the species

Chapter 4:  Mutation, genetic variation
There are various types of genetic change:
• Point mutations (changes from one base to another)
• Insertions & deletions (of base pairs)
• Gene duplication
• Chromosomal inversion (flipping of segment)
• Polyploidization (doubling of chromosome number)

Fig. 4.1

Fig. 4.4. Transitions outnumber transversions, often by >2:1

What causes point mutations?
• Mistakes in DNA replication
• Damages (as from radiation) that are not correctly repaired
(Mutation does not respond to specific ‘needs’)
(Some mutation is inevitable)

Fig. 4.3
So … Some point mutations change the amino acid (replacement substitutions),
while others do not (synonymous substitutions).
The latter are presumably nearly neutral.

A second type of mutation is an indel,
that is, an insertion or deletion of a base pair.
If other than 3 base pairs at a time are inserted or deleted,
then there is a frameshift.  This results in loss of function,
or is a sign that function was previously lost.

So, what are common mutation rates?
• Until recently very hard to estimate for the various classes of mutations (synonymous/replacement; indels…)
• But, you’ll hear numbers like 1/100,000 per gene copy per generation that are loss of function & observable.
• This is a lot in a genome of 30,000 genes (the book assumes 80,000):
2 x 30,000/100,000 ~ 0.6 per generation per genome.
(The 2 is because there are 2 gene copies at each locus, or equivalently because we all come from one egg + one sperm.)

• Newer techniques get at the rate per nucleotide site.
• For C. eligans, could be 15 new mutations genome-wide
per generation (most would have to be neutral).

What is the distribution of effects?
• Only a tiny fraction are advantageous.
• Probably a huge number are nearly neutral.
• And a substantial number are deleterious.

Where do new genes come from?  Old genes are duplicated.
Can happen through unequal crossing over during meiosis…
Fig. 4.7

Fig. 4.9

Chromosomal alterations
• Lots of kinds, but one to remember is an inversion (flipping of a chromosome segment - the order of genes is altered)
• Inversions generally prevent crossing over and recombination alleles are locked together as a unit.
• They tend to adapt to local conditions, then form clines along environmental gradients (like latitude)

4.11. Drosophila subobscura was recently introduced in the NewWorld, then reformed its clines just like in Old World

Polyploidy (4.12)
• The whole genome is doubled, so 2n fi 4n.
• Doesn’t seem to work much in animals.  Very common in some groups of plants.
• Instantly makes new “biological species”; later they can diverge in morphology, ecology, etc.

• Point mutations … creates new alleles
• Indels … frameshift makes nonsense, or amino acid gained/lost
• Gene duplication … the extra gene is free to evolve new function
• Chromosomal inversion … prevents recombination within
• Polyploidization … one way new species arise (not only way)

New Topic:  Genetic Variation in Natural Pops
• Classically expected to be low - one allele should be better than all others and selection should keep deleterious ones at very low frequencies.
• But … electrophoresis of enzymes overwhelmingly found lots of variation.
• Two explanations:  (1) could be neutral; (2) could be selection favors different alleles at different times and/or places (big controversy in the 80’s).
• Now even more variation is evident at the DNA level.

Fig. 4.14

Heterozygosity (H):  average frequency of heterozygous loci (Fig. 4.16)

Chapter 5:  Mostly selection on one locus
Microevolution - change in allele frequency over generations
Macroevolution - change in taxon diversity in phylogenies and biomes over time
Sex - n. the systematic recombination of genetic elements through meiosis and fertilization

The gene pool (5.2)

Fig. 5.3. evolution happened, due to genetic drift

Fig. 5.5. Now, do it with no randomness…(Fig. 5.6)

So,
• Sex by itself does not change allele frequencies
• When the assumptions hold, the diploid genotypic frequencies are p², 2pq, and q², respectively of freq(AA), freq(Aa), and freq(aa)
where p is the frequency of A, and q is the frequency of  a in the gene pool

Assumptions of Hardy-Weinberg equilibrium (Fig. 5.10)
• No selection (or linkage to selected loci)
• No mutation
• No migration
• No chance events (infinite population)
• Random mating
H-W is the null model

Selection happens when individuals with particular phenotypes survive at higher rates than ind’s w/ other phenotypes, or
when ind’s w/ particular phenotypes reproduce at higher rates than ind’s w/ other phenotypes.

Selection on the basis of phenotypes has consequences for frequencies of genotypes, but there need not be a 1:1
correspondence between genotypes and phenotypes …
      • Dominance and/or epistasis (non-additivity) can complicate (weaken) the response to selection.
      • Less than 100% heritability can weaken the response to selection.

Adding selection to the model…Imagine p=0.6, q=0.4
                    at birth               after selection
freq(B1B1) =  36                            36           
freq(B1B2) =  48  …  kill 25% …  36
freq(B2B2) =  16  …  kill 50% …    8
p’ = 0.675, q’ = 0.325

Fig. 5.11

Fig. 5.12. Modest selection over a 1000 generations can move p from 0.01 to 0.99 … but just wait until we get to the many loci model.

5.13. Selection in the lab … example could be through survival or reproduction.

Strong selection can also throw off the H-W frequencies
Let p=0.5
                before selection           after selection
freq(B1B1) =  25   …   kill 60%  …  15 ≠ p²
freq(B1B2) =  50 let them all live … 50 ≠ 2pq
freq(B2B2) =  25   …    kill 60%  … 15 ≠ q²
p’ still = 0.5
You may find a deficiency or an excess of a particular diploid genotype (selection is one but not the only possible cause).

Making a bunch of simplifying assumptions, could you have evolution in 1000 years for HIV resistance? (Fig. 5.15)
Yes, but only if you started with initial freq’s the highest recorded, and with selection the strongest recorded…

Play with AlleleA1 simulation for a while … demonstrate
1. Advantageous new mutant recessive alleles take a long time to rise from 1% to modest frequency
2. Advantageous new mutant dominant alleles take off quicker but then drag later on near fixation
3. Maximally addiative fitnesses have the quickest evolution
4. All of them evolve a lot in 1000 generations
5. Heterozygote superiority results in a balanced polymorphism
6. Homozygote superiority means that the initial frequency matters
7. Mutation can cause very slow (non-adaptive) evolution by itself
8. With selection mutation can be the rate limiting step
9. Very small populations drift faster, but all finite populations drift eventually

Effect of dominance:  slows down evolution when the recessive allele is rare
The spread of a new recessive mutation is much slower than the spread of a new dominant mutation (or of a codominant mutation)
Selection has a hard time eliminating the last copies of a deleterious recessive allele (if q=1/100, then q²=1/10000; which is why all populations of diploid eukaryotes have a bunch of rare genetic diseases, or in other words, carry a genetic load)

• Heterozygote superiority is when A1A2 are more fit than either A1A1 or A2A2 -> intermediate stable equlibrium p
• Selection favoring homozygotes -> which allele goes to fixation and which is lost depends on initial frequencies
• Frequency dependent selection (elder flower e.g.) -> balanced polymorphism

When you have mutation…
• If mutation from A->a is more common than backmutation a->A, over thousands of generations the population will evolve toward a (mutation by itself can account for evolution over the long term…evolution toward disorder)
• Mutation rate can limit response to selection’s rate if the selection regime has persisted for a long time; mutation provides the raw material for selection to act upon
• There is a mutation-selection balance by which (the equilibrium frequency of a deleterious allele is the sqrt of the mutation rate / selection coefficent)

Is the frequency of cystic fibrosis explicable by mutation-selection balance?
No:  it’s q=0.02, so µ would have to be 4/10000 It’s probably been selected for (in heterozygotes) during typhoid epidemics (Fig. 5.27)

Chapter 6

Migration (gene flow)
• Algebraically, it’s a lot like mutation, but the frequency of new migrants can be anything (higher or lower than mutation)
• In looking at natural populations, migration is one explanation for homozygote excess (two populations that are differentiated partially mixing in one’s sample)  Others are…
• A common effect of migration is to homogenize subpopulations that would otherwise differentiate under drift or local adaptation

water snakes: Fig. 6.7: Some banding persists on the islands because of gene flow from mainland

Finite populations -> genetic drift (changes in allele frequency due to random sampling of which gametes make it into the next
generation; something analogous could also happen for asexual ‘populations’)
• Imagine going through the life cycle with N=10
• Then imagine doing the same thing for all different N: The larger N gets, the less probable drift is
• Founder effect (also bottlenecks):  population goes through some generations of small N

Silvereyes show the effects of a series of founder events (Fig. 6.13)

Fig. 6.15
• Every pop follows a unique path
• Drift goes faster w/ small N
• Given enough time, p can change a lot even with N=400
•Prob(A1 goes to fixation)=initial freq

Fig. 6.16. Now consider a whole set of populations (each of 16 flies)
Some will drift to one absorbing boundary (fixation of one allele). Some will drift to the other boundary (loss of that allele)
AVERAGE heterozygocity will decline to 0

Fig. 6.17. Look the 107 pop’s lost H faster than they should have; their effective population size N_e=9, not 16

Drift very interesting in conservation biology
Populations have recently been fragmented (lost gene flow), and been made small pop’s become genetically depauperate, suffer inbreeding depression, lose the ability to adapt to changing environments … bad, bad, bad

Collared lizards in glades in the Ozarks (6.18).
Agriculture, abandonment, fire suppression
oak hickory ‘ocean’. red cedars in glades. monotony w/in pops
At Stegall Mt, controlled burning -> lizards migrating between glades, colonizing new glades, return of heterozygocity

I can’t resist one more example: Fig. 6.19 shows that genetic polymorphism and allelic richness
is related to N (for marker enzymes)

Wright, Haldane, and Fisher (and others) derived this really elegant theory on the assumption of Mendelian inheritance, the theory of population genetics.
• You can understand it with high school algebra
• It accurately predicts evolution in experimental pop’s
• Now that we have molecular markers, it provides a working knowledge of the study of variation within and among pop’s (relevance for epidemiology, conservation, agricultural, reproductive biology…)
It starts with understanding Hardy-Weinberg, then adding selection, mutation, migration, drift, and non-random mating

What’s happin’
1. Deleterious alleles appear and are eliminated by selection
2. Neutral mutations appear and are lost or fixed by drift
3. Advantageous alleles appear and are swept to fixation by selection
For DNA point mutations and amino acids, there’s a long debate between neutralists emphasizing #2 and selectionists
emphasizing #3
Neutralists, notably Motoo Kimura, built off of Wright and developed a whole (null) model of math for molecular variation

Neutral theory of molecular evolution … which then became the null model of molecular evolution…

Fig. 6.20

The substitute rate = neutral mutation rate
It’s independent of N:  in small pop’s there’s few mutations but those that occur are more likely to be fixed; in large pop’s there’s more mutations but they’re more likely to be lost
Allopatric pop’s inevitably diverge through the accumulation of neutral substitutions (as well as, of course, selective sweeps)

Neutral theory is the starting point for understanding evolution of pseudogenes, non-coding regions, and synonymous changes
These rates are then the yardstick for studying a.a. replacement changes. Fig. 6.21

Actually, synonymous substitutions are not totally neutral…Codon bias can cause weak selection (some tRNAs are more available than others; efficiency of translation can be affected)

• Rates of change are remarkably high (too high to be due to positive selection)
• Rates of change, especially in silent regions, are often fairly clock-like on a per-generation basis
• Replacement changes are better standardized on a per-year basis, invoking the nearly neutral model mutations are effectively neutral when the selection coefficient is less than 1 over 2N_e
 
Certain types of loci seem to have been under strong positive selection
• Recently duplicated genes that have taken on a new function
• Genes involved in fertilization (sperm/egg recognition)
• Genes involved in disease resistance (immune system) etc.
Other loci seem to have more neutral evolution
Conclusion:  The genome shows signs of a lot of positive selection, but there’s so much variation that there’s plenty of room for neutral and nearly neutral evolution at the molecular level

Non-random mating does not by itself change allele frequencies
It does change the eq. genotypic freq’s (≠ p²+2pq+q²): e.g., selfing reduces heterozygosity by 1/2 each generation
In combination with selection against homozygotes (inbreeding depression), it sets the stage for adaptive evolution in mating systems

Usually, when you have inbreeding there is a reduction in fitness, called inbreeding depression
It’s worse in harsh environments
It’s mostly due to exposing deleterious recessive alleles
Some spp. self habitually tending to be purged of deleterious recessives

Figs. 6.3 & 6.31. Effects of drift -> fixation of deleterious alleles, i.e. inbreeding depression

Chapter 7

Linkage disequlibrium - a non-random association between the alleles at two loci (Fig. 7.2)
• Could involve physical linkage on a chromosome, but that’s not in the definition

What causes linkage disequilibrium?
• Mating that is non-random with respect to the two loci
• Multilocus selection
• Drift
• Population admixture
What diminishes it?
• Recombination (Fig. 7.6)

When two loci are in linkage disequilibrium, selection on one locus can change the allele frequencies at the other locus (Fig. 7.8).
• There must be serious physical linkage for this kind of hitchhiking to be a major complication … or else there’s some other reason for an unusually low amount of recombination.

Finally…What is the function of sex?
Remembering, sex to a geneticist is the systematic recombination of genetic elements through meiosis and fertilization, connotes
• Meiosis with crossing-over
• Outcrossing (easiest to start thinking about with gonochors like ourselves, but then there’s hermaphoditic plants…)

Ancillary costs associated with sex
• you may not find a mate
• searching for a mate takes time and energy
• you risk predation, and sexually transmitted diseases
• the mate may demand courtship exertions
• it may not work

Outcrossing is expensive … there’s the demographic “cost of males” (Fig. 7.17)
…a 2-fold advantage in organisms where males don’t invest in offspring and sons cost the same as daughters
But the vast majority of organisms have sex at least occasionally
Here’s an example of a sexual form winning out over an “asexual” form despite a 3-fold disadvantage (7.18): Was the sexual form evolving a strong competitive advantage?

And after artificial selection experiments, one sees an increase in the ability to recombine (7.19)

At the level of population genetics, the only consequence of sex (s.s.) is the reduction of linkage disequilibrium
• A model for the benefit of sex must include (1) a mechanism that eliminates particular multilocus genotypes or produces others, thereby creating linkage disequilibrium; and (2) a reason why recombination is favored
1. Muller’s ratchet - slowly drift makes the multilocus genotypes function less and less well.  Explains on a broad phylogenetic level the maintenance of sex
2. Selection in ever-changing environments - when there’s a trade-off between being adapted to one environment versus being adapted to others, sex recreates favorable multilocus genotypes; the genes for recombination ride to high frequency in the high-fitness genotypes that they help to create.  Explains the short-term benefits of sex

Environments might be ever-changing because of parasites or competitors.
7.23. Pop’s with lots of parasites have fewer asexual snails

These models help explain the maintenance of sex
• Basically large eukaryotes have evolved a genome that is addicted to sex - without it lineages tend to go extinct
• And in the world of the Red Queen, where everyone has to keep running and running just to stay in one place, it behooves mothers to make variable offspring.
This does not speak to the original origin of sex at the base of the eukaryotes

Chapter 8 - evolution of quantitative traits

• Everything in Ch. 5-6 was about traits that vary because of single loci; actually many (¿most?) of the features of
evolutionary interest are influenced by many genes and many aspects of the environment

Fig. 8.2. How many particulate loci make for a quantitative trait

Fig. 8.3
• The range in the F₂s doesn’t extend to the full range of the parentals
• But selection can recover the full range (the alleles abcdef and ABCDEF still exist)
• Actually, even in the pure parents of most wild pops there would be scattered variation that selection could
bring together (the magic of recombination)

QTL studies (Quantitative Trait Loci)
• With molecular markers, make a map of the genome
• Measure traits in F₂ array
• See how traits are associated with each marker (linkage group)
Fig. 8.8 Surprisingly, in monkeyflowers, 1-3 QTLs explain much of the difference between spp.; it’s not infinitesimal

Knowing something about molecular mechanisms can help to find candidate loci …

heritability (h²=Vadditive/Vphenotype)
• p. 303, 3rd & 4th ¶
Vphenotype=Vgenes + Venv
                      Vgenes = Vadditive+Vdominance+Vepistasis

Fig. 8.13

Several ways to estimate h²
• parent-offspring regression (8.12)
• twins
• h² = R/S

S:  selection differential, traitafter - traitbefore
Fig. 8.15

Fig. 8.18

evolution is  R = h² S
  R:  response to selection (evolution)
  h²:  narrow-sense heritability, V_additive/V_phenotype
  S:  selection differential, trait_after - trait_before

…So far, we’ve talked about direction selection, but…Fig. 8.23

Evolution by selection:
(1) variation exists
(2) some of it is heritable
(3) some individuals are more fit than others
(4) some of that fitness is due to phenotype
This can result in evolution
We say it “can” rather than it “does” because 4 does not specify directional selection.  Stabilizing or disruptive selection might not result in evolution, though it certainly has interest for evolutionary biologists.  E.g., stabilizing selection is our 1° explanation for stasis, disruptive selection is important in some mechanisms of speciation

Fig. 8.24. …acting on gall size, two agents of selection cause stabilizing selection

…disruptive selection can explain polymorphisms and more generally alternative phenotypes… (8.25)

There’s a lot of genetic variance in most natural pop’s. Why?
• On the way to some new and more apt state
• Genetic load, caused by slightly deleterious mutations
• Heterogeneities in the selective regime


This is where the notes for the 2nd exam start

Chapter 9: F&H’s points:

• One should explore a series of alternative hypotheses (giraffe example)
• Experimental studies allow one to relate components of fitness to traits.  One can manipulate the phenotype for one character independent of other characters (wing-waving in tephritids). One can vary the environments
• Observational optimality studies.  Do the organisms behave or have characters that can be shown to approximate the optimal state? (thermoregulation example)
• The comparative method.  Is a character correlated across species with another character or environment (bat example)

Fig. 9.6. Tephritid flies. The patterns currently function to deter predators (jumping spiders)


Fig. 9.8. The animals find spots with temperatures close to their optimum

Fig. 9.12. Correlations across spp. may seem strong when they are not well supported because of phylogenetic non-independence. This problem can be accounted for using phylogenetically independent contrasts (Fig. 9.13). Also, there’s all sorts of other cool statistics for studying other aspects of the historical pattern,
e.g., whether one character tends to evolve before or after another character

Fig. 9.14. Bat example

Then see handout

An adaptation is a feature that was formed during history by selection because of a benefit conferred in a specified function. (The word for has an unfortunate whiff of teleology … but se la vi.) It is helpful to sketch out the prepositions that specify the form of natural selection on traits, via components of fitness, among individuals, and by agents of selection.

Many biologists do not define adaptations in this way.  When they say, “Stump sprouting in sumacs is an adaptation for surviving frequent fires in the Mediterranean climate of California. ” they might mean is serves that purpose regardless of how it was formed. They use the word ahistorically.

An exaptation is a feature that has been co-opted for a use that did not drive its origin.

Not all features of organisms are adaptive at all:
•The fall of the flying fish
•Correlated response to selection
•Genetic drift
•Historical artifact

In my world, the study of adaptation must be hypothetico-deductive.
(a) One could gather additional data by studying how selection works in similar contemporary systems or how characters are apt by surgically modifying them.
(b) Adaptive hypotheses are often tested by studying how adaptive complexity is organized around a way of life; one might show that several aspects of the organism match optimal specifications dictated by one another, or that a quantitative character is optimal given other characters.
(c) Using phylogenies (which on occasion are based on fossil as well as extant organisms), one may show comparative patterns in which there are correlations between the character of interest and the environment that is thought to favor that character, which is best done with analyses that take into account the polarity of character change and which changes occur first versus which subsequently.
Not being able to directly see generalities, basing generalities on weaving together specific information, and the tenuous induction of specifics from generalities even when true – all these are common features of scientific knowledge, not confined to evolutionary biology. 

Demonstrating the truth of an historical explanation is not the only reason to think about adaptations.  A second reason is that we further our understanding of evolutionary processes, which would seem to be of overriding intellectual interest, and a third reason for studying evolutionary causes is that by doing so, we further our understanding of the biology surrounding whatever we are studying. 

Ch. 9 continued
Examples of ultimate explanations
• Phenotypic plasticity, adaptive?
• Tradeoffs and constraints in floral adaptation
• Genetic variance Y/N?  Host shifts in beetles

Fig. 9.17. Is phenotypic plasticity adaptive in daphnia? Notice the variance in differences between blue and red; some clones more plastic than others. The most plastic were from the lake with fish present

tradeoff - becoming good at one thing make the organism bad at another thing (big flowers makes for few flowers)

constraint - a more general idea - the functional features of the organism dictate which evolutionary paths are “easy” and “hard”, “possible” and “impossible” (the time it takes pollen tubes to grow requires that fuchsias not abscise the flowers, so they evolve to be a different color: Fig. 9.20)

Fig. 9.21, Table 9.4. Lack of genetic variance can constrain host shifts
Beetle tested for feeding on a plant that is
…in the same tribe as its host:  88% genetically variable
…in a different tribe:  45%
Beetle tested for feeding on a plant that is
…the host of a closely related beetle:  75%
…the host of a distantly related beetle:  38%

Ch10 Sexual selection

Bateman’s principle: sperm are more numerous and cheaper  than eggs, so a few males can sire more than their share of offspring, implying, male reproductive success can be more variable than female reproductive success. Sexual selection acts more on males than on females. Males are the absurd sex (Fig. 10.3)
There are exceptions that improve the logic. The gender with the lesser parental investment is the most subject to sexual selection (females in seahorses, phalaropes). When both sexes invest heavily, or in monogamous species, things become more complicated, and sort of more equal.

Fig. 10.5. newts and pipefish

Fig. 10.8. marine iquanas…The males get to be bigger than is ‘good’ for their survival.
Fig. 10.10. #59 was largest male, ejected 4 other males, lost parts of territory to 4 other males.
                                           Santa Fe    Genovesa
males that copulated    SVL=401            243
males that tried                      390            227

Fig. 10.12. dominant males and sneaker males, alternative male mating strategies

Fig. 10.13. Med flies…raised & mated alone:  1379 sperm. Raised & mated with other males:  3520

Fig. 10.14. damselflies…removing the last guy’s sperm.

Lions:
• male coalitions form and battle with other coalitions that have prides (coalitions are usually of related males, not related to the females)
• coalitions only hold on to prides on average for 2 years
• when a new coalition takes over, they kill the kittens (who were presumably sired by the last coalition) … (this accounts for 25% of kitten deaths, 10% of all lion mortality - it isn’t ‘good for the species’)
• females abort fetuses of previous coalition:  they would be killed anyway, so it’s not adaptive to waste energy on them

Female choice
• Darwin wrote about it extensively
• Not taken very seriously until ~1970 (1966)
• Explosion of interest since then
How did it evolve?
• Good genes
• Direct acquisition to resources
• Pre-existed as a sensory bias (related to other choices)
• Runaway sexual selection between choice & male CHR
(none of these are mutually exclusive)

Barn swallows
One might not think a great candidate…
• Both parents invest
• At first glance monogamous
But males have longer tails (Fig. 10.16)
Fig. 10.17, Table 10.2
extra-pair copulations by males:
         0       0       0       0.040
by their female pair-mates
     0.036  0.014  0.017    0

Fig. 10.20. Gray tree frogs
Fig. 10.21. Females prefer long-calling males
For various measures of performance, the long-callers sired better off-spring (Table 10.3)
Evidence for good-genes hypothesis.

Fig. 10.22. Hanging flies:  males give nuptial gift. The bigger the gift, the longer the copulation allowed by the female and the more sperm are transferred, up to a point
So, females may be choosybased on what resources they receive. Then the male may break it off and use the remaining food to attract another female

Fig. 10.23. Pre-existing sensory biases in females water mites:  the female senses the male in the same way she senses prey; males have been selected to do ‘trembling’
Fig. 10.24. netstance and trembles could have arisen in the same segment, but…it’s plausible to imagine that N arose first, and caused selection for T

Runaway sexual selection: Once there’s some female choice, then females who choose will have sexy sons who will sire more than their share of grand-daughters who will tend to be choosy…

Fig. 10.26, 10.27.

Main ideas
• Sexual selection will proceed until it is countered by survival selection
• Although male-male competition is called intrasexual selection when females choose, they are also choosing among males (so ‘intersexual selection’ is a misnomer.  Better terminology:
                       male-male interference competition
                       male resource usurpation that leads to female choice
• The form of sexual selection depends on parental investments and on who controls what (and whom)

Darwin set forth these ideas in The Descent of Man, and Selection in Relation to Sex. He was obviously suggesting that human evolution has been shaped by sexual selection - this turns out to be in ways that are very complicated and require an understanding also of kin selection and social evolution

anthropomorphism - making something seem human (that oughtn’t to be), e.g., making an animal seem as if it has conscious intentions when it may well be following fixed action patterns
teleology - reading purpose, intent, design into the features of the natural world, e.g., making adaptations seem as though they are for a purpose and reveal the intentions of a designer
typology - treating the essential type of something (a species) as though it were real, more real than the flawed instances.  Actually the characteristics of a taxon should be thought of like averages, ‘unreal’ summarizations

Ch. 11. Kin selection…
• Explaining altruistic adaptations
• How selection shapes CHRS in individuals for the benefit of kin
• Hamilton’s rule:  An altruistic feature will be selected for if the cost to the actor is less than the benefit to the recipient times the coefficient of relatedness:  C < B·r (i.e. if B·r-C>0)
• coefficient of relatedness, r:  probability that gene copies in two individuals are identical by descent (Fig. 11.1)

In other words, selection favors traits that maximize inclusive fitness, which is made up of direct fitness + indirect fitness. The relationship between the character and the indirect component is kin selection.

Belding’s ground squirrels. Whistle when hawks approach; trill when coyotes etc. approach. Whistling appears to benefit self:  2% get eaten versus 28% of (inattentive) non-whistling squirrels. trilling, though, appears to be altruistic:  8% get eaten versus 4% of non-trillers. Most alarm calling is done by females (Fig. 11.2). Trillers more likely to give alarm call when close relatives are around (Fig. 11.3)

Bee-eaters, example of cooperative breeding, which seems to happen when breeding opportunities are capped in number (e.g. only a few places to nest, but lots of food and work at each place) probability of helping at nest depends on relationship to beneficiary (Fig. 11.6). Fig. 11.7. Fitness gains due to helpers helping

Tiger salamanders prefer to cannibalize non-relatives. Fig. 11.8. Relatives would be just as nutritious…if only they were as delicious

Fig. 11.10. American coots:  conspecific nest parasitism selects for discriminating one’s own eggs from other’s eggs. not discriminating costs them in future clutches. and they do discriminate to some extent

J. B. S. Haldane:  “I would be willing to die for two brothers or
eight cousins.”
• One mechanism for the evolution of altruism is kin selection
• Notice that although individuals are fashioned into altruists, the alleles that affect these traits are being ‘selfish’ - favoring the spread of themselves
• Once altruism gets going, it becomes adaptive to know who is kin if possible and to masquerade as kin if possible
(Nothing about this is very comforting:  evolution favors selfishness and nepotism …)

eusociality: (1) specialized non-reproductive castes,
                    (2) cooperative brood care
                    (3) overlap in generations
the extreme of reproductive altruism
has arisen many times in the Hymenoptera, a few times in other insects, in snapping shrimp, and in mole-rats
In the Hymenoptera, haplodiploidy could pre-dispose the evolution of eusociality

haplodiploidy:  males are haploid (from unfertilized eggs), females are diploid (Fig. 11.12)
full sisters r=3/4
mother to a daughter r=1/2
sister to brother r=1/4
So, if the sex ratio is female biased, it’s better to raise sisters than daughters
Most eusocial Hymenoptera do have female biased sex ratios (but is it cause or effect?)

haplodiploidy is probably part of the explanation, but only part
C and B are just as important as r
(remember altruism only evolves when Br>C)
there are lots of hymenoptera that are not eusocial
fancy nesting arrangements seem to be a pre-cursor to eusociality. Fig. 11.13.

Naked mole-rats:
• Resources (burrowing sites with tuberous plants) very patchy
• Extreme inbreeding, so r is large
• Other mole rats have overlapping generations and material care
The queen is larger than the workers
She literally shoves them around (less so if they are very closely related), and nips them into working
(Fig. 11.16)

Parent-offspring conflict, e.g., when to wean (Fig. 11.18)
mothers should wean after the costs outweigh the benefits; offspring would like to wait until the costs are 2x the benefits, when it becomes better to have a full sibling

back to bee-eaters: when a young male tries to get a territory, often his father harasses him … and often the young male gives up and returns to his parents’ territory to help them raise younger sibs
Fig. 11.19. ‘risk of recruitment’ is probability of getting hooked into helping at relatives’ nest

reciprocal altruism: book plays it down and splits hairs not counting instant ‘byproduct mutualism’, but I have a feeling it’s
happening in complex societies when:
• each indv repeatedly interacts with the same set of indvs
• opportunities for altruism are frequent during the course of an association
• animals have good memories
• positions change frequently
• costs less than benefits

vampire bats:  starvation is a real danger, but when you find a cow the blood is plentiful (Fig. 11.22)
multiple regression indicates both effects significant accounting for the other

FRIENDS AND RELATIONS ARE IMPORTANT IN THE EVOLUTION OF ALTRUISM
The individuals behave altruistically, but the genes are always being ‘selfish’

Ch12:  Life history evolution
• generally about the evolution of aspects of life tables and the 'economy of life’
• due to the constraints in how to deploy time and energy, tradeoffs lead to alternative strategies
long-winged crickets can disperse better short-winged crickets can produce more young (Fig. 12.3)
• we start with an explanation for the evolution of senescence

senescence is an acceleration of the rate of mortality with age, or at least a decline in the rate of fecundity (Fig. 12.4)
life tables emphasize fecundity m_x and survivorship l_x a population’s life table statistics are just as subject to natural selection as its teeth and claws.  (Notice, though, the best way to understand these CHRs is by thinking about the population.)

First, the rate-of-living hypothesis for senescence
• cell lines may only have so much ‘life’ in them, whereby the faster they metabolize, the sooner they die
Fig. 12.7
It’s an idea that won’t seem to go away (there’s lots of data on it from cell biology), but animals are variable in life-time energy expenditure, and response to selection experiments show life can be extended (Figs. 12.5, 12.6)

rate-of-living may be helpful as a proximate explanation
but a winning evolutionary explanation comes from
Medawar 1952 … accumulating of late acting deleterious mutations
Williams 1957 … antagonistic pleiotropy

Fig. 12.9 a versus b. Remember selection-mutation balance and genetic load. Well, deleterious mutations late in life (after the organisms have usually done most of their reproducing) have very little effect on fitness and so the equilibrium qs are larger.

increase in inbreeding depression with age consistent with the idea that there might be high frequencies of deleterious late-acting mutations (Fig. 12.10)

Fig. 12.9 a versus c. a mutation that is a little bit beneficial in youth will be selected for even if it is lethal in old age

hx546 allele causes increased longevity. But under stressful conditions it evolves to quickly to low frequency (Fig. 12.12), so it must be beneficial in some other component of fitness, i.e. life table statistic

Fig. 12.14. Opossums on a predator-free island and adjacent mainland

Why do we deteriorate in old age?
because selection doesn’t care so much about individuals who (a) have a greater chance of being dead by accidents and (b) who have done most of their expected reproduction. Moreover because (c) we are adapted to have a good time on average when we are young and that comes at a cost because of physiological, physical, and temporal tradeoffs

Lack’s theory of optimal clutch size (Fig. 12.16)
if a bird lays too few eggs, then opportunity is lost. if a bird lays too many eggs, then they can’t all be raised

however, generally, birds lay slightly fewer than they could fledge (12.17)
why?
• saving some energy for the next clutch
• doing a good job a raising healthy fledglings
• for parasitoid wasps, to save time looking for another host
(notice the iterative adjustments in theory that are yielded by the scientific method.)

Fig. 12.22. How big should offspring be?
• assume a tradeoff between size and number
• assume fitness of offspring is a decelerating function of size
And you get:
what is optimal for the mom is not optimal for an individual offpring

Fig. 12.23. Look, it works for salmon in hatcheries their eggs are evolving to be smaller make the theory a little more elaborate for two environments (12.24)
Fig. 12.25. For beetles on Acacia (good host) and Cercidium (poor host). they show apt phenotypic plasticity, at least when moving to the poor host

Bottom line on life history evolution
physics, time constraints, and how the organism works (physiology) cause there to be tradeoffs between different life history variables
local populations adapted one way or the other
species diversity is found along these tradeoff envelopes

Ch 13:  Evolution and human health

flu: niffty example of how phylogenies can be informative (13.4)
evidence of recombination (13.5)
The 1968 epidemic seems to have an H3 gene from a bird virus. Could have recombined with human virus in a pig (Fig. 13.6)

Antibiotic resistance
• evolves through many molecular mechanisms
• selection  is hard to avoid (somewhere there’s going to be a place where some can live and others are dying)
• innumerable examples - often happens within decades
• initially it comes at a cost such that in the absence of antibiotics susceptible genotypes are favored, but eventually this is selected out and resistant ones are just as fit even in the absence of antibiotics
early in the evolution of resistence, the tradeoff selection favor reversal; later, after the genetic background has coadapted the tradeoff disappears
So, take your full course and use antibiotics only when necessary

evolving pathogens
• they have short generation times, so they can adapt faster than their hosts
• large population sizes, also, tend to make for easy adaptive evolution
however, patchy genetic structure (one founder) can make for higher level selection

virulence: harm done by a pathogen to its host: • stupid, right?  •no, could be adaptive
evolutionary dynamics depend on
• whether there are often multiple infections - if pathogen particles are not all related, then the one that uses up resources the fastest is selected for
• mode of transmission - if to get on to the next host it must keep the current one healthy, then it evolves to be non-virulent
Fig. 13.10. vectorborne diseases are more likely to cause death directly transmitted pathogens are selected to not incapacitate host
Fig. 13.11. waterborne diseases are virulent

Consider our environment of evolutionary adaptation
• for 99% of human history we were hunter-gatherers
• got plenty of exercise, lots of squatting
• ate no grains, milk as adults, refined sugar, not much fat, alcohol
• not too much close visual work
• women often pregnant or lactating
There hasn’t been all that much time for us to adapt to urban conditions

Is fever adaptive? (Fig. 13.19)
• behaves like it is
• seems to have benefits in lizards with infections
remarkably few studies on if and when suppressing fever with drugs
is really suppressing ‘the wisdom of the body’.

Parenting?  Do humans discriminate based on r?
Reed bunting dads do (13.22)
So do dads in the Caribbean (13.23)
spend more time with genetic offspring
and are less likely to yell at them
(Results can’t be explained by age given other results)
and how do step-children fare? Fig. 13.25
okay, none of that was very abnormal, but look at the relative risks of children being killed by a genetic versus a step parent (Fig. 13.26)

Many of these conclusions about humans are sketchy
But it’s not been a cottage industry to apply evolutionary thinking to human health and welfare. Much more research is warranted. Early results are intriguing.

See handout introducing phylogenies.

if there were no homoplasy, inferring the tree would be easy, but…you never know for sure before you have the tree that any similarity is
a homology (Fig. 14.3). solution:  get a ton of seemingly independent characters and go with the preponderance of evidence on the argument that
common ancestry is the cause that most coordinates nested patterns of similarity

Several methods for inferring trees:
parsimony - the tree that requires one to postulate the fewest evolutionary changes
maximum likelihood - a tree that models the process of (molecular) evolution (estimating rates of transitions, transversions, etc.)
distance (neighbor-joining) clusters - puts together based on similarity and dis-similarity, works best for clock-like evolution

parsimony
• An exhaustive search (a) draws out every possible tree, (b) maps all characters onto each tree, and (c) you take the shortest tree
• When you have lots of taxa, though, this is prohibitive, so you have to explore tree-space, and then optimize from short trees that you stumble upon

only for the purposes of illustration, consider just two trees…Fig. 14.4
artiodactyla hypothesis implies 47 steps, the whale+hippo 41 steps (Fig. 14.6)
but is this really convincingly more?
bootstrapping can help you quantify your confidence
the computer resamples your data, making (say) 1000 resampled data sets; each on is used to infer a phylogeny; you then ask how many of the phylogenies have each monophyletic group in your best phylogeny
i.e, how consistent are the data with each other in giving a particular answer
people often take 70% bootstrap values as ‘reasonable’ confidence in an answer for the whale+hippo data, bootstrap support ~100%
At this point, there’s a well-supported hypothesis, but it still deserves to be critically tested with new data
Fig. 14.8. Sort or Long INterspersed Elements (SINEs and LINEs) parasitic genes that insert themselves in the genome at a low rate, so convergent gains are very unlikely, and when they are lost they usually take some stuff with them in a unique way, so convergent losses can be detected
So the molecular evidence is unanimous
14.9. And then fossils were found that have the ear bones of whales and the angle bones of artiodactyls…This doesn’t really address which artiodactyls
It would be nice to find some protohippos from about 50 million years ago

What are the phylogenies good for?
• Establishing polarity
• Classifying … organizing … but this would be not perfectly traditional
• Distinguishing homology from analogy
• Narrating the history of adaptations and carrying out the comparative method
• Molecular clock stuff - dating either relative or calibrated, what radiations happened fast or slow, when was the common ancestor of all the people alive today?
• Biogeography - how did lineages radiate as geographic barriers rose and fell, dispersal events happened, etc.
• Cospeciation versus host shifts (figs, pathogens, herbivores)
Fig. 14.10
Fig. 14.12. Ostracod eyes convergent gains or repeated losses?
Fig. 14.14
phylogenies are your friend


This is what you need to study for the 3rd exam (given during the final time).

Ch. 15:  Speciation
• F&H’s treatment skimpy, so look out for extras…
• Along with explaining adaptations, explaining diversity is central to evolutionary biology

Outline:
• Species concepts
    -Taxonomic (morphological) species
    -Biological species
    -Phylogenetic (geneological) species
• Three stages that can but need not be in order
    -Isolation (extrinsic or intrinsic)
    -Speciation (origin of reproductive isolating barriers)
    -Reinforcement, which might be rare
• Genetic basis of speciation
    -pleiotropy between what & what?
    -few or many genes?

The word ‘species’ has multiple meaning, so beware
species (1) a taxon at the rank above subspecies and below genus; (2) the thing that is the result of speciation; (2a) something that has come to be unable to interbreed well with other such groups; (2b) something that has a substantial history of not interbreeding with other such groups

It’s like the word democrat - it could mean someone who believes that decisions should be made by each person having a vote, or it could mean something rather more derived and difficult to explain

species concepts, though they may be practical criteria for recognizing taxonomic species (#1), more importantly they are interesting because they structure our thinking about speciation (#2)

Taxonomic (morphological) species
•It’s whatever a competent taxonomist proposes and other competent taxonomists see no reason to revise
•Sounds like a cop-out, and certainly strips species of deep meaning, but works surprisingly well
    -folk taxonomists from many cultures agree
    -has proven exceedingly useful in predicting
    evolutionary conservatism in sexual organisms for traits     not even used in the original circumscription
•Often comes down to multiple (two) traits showing discontinuities in dividing up organisms into the same two sets

Notice we would get into huge political trouble if we did this to humans
• humans are a pretty unusual case (human ‘races’ are not distinct)
• but the main reason is because ‘species’ has a typological meaning in our culture
• to working taxonomists the designation doesn’t mean much more than ‘a sort-of kind-of distinct group’; remember this when you use the names that taxonomists have given us (some taxonomists do try to make it mean more, and they end up with subspecies, varieties, formae, etc.)

F&H say:
A species is the smallest evolutionarily independent unit. Evolutionary independence occurs when mutation, selection, gene flow, and drift operate on populations separately.
Debatable…
but let’s say you went with this.  Then various human populations are obviously not independent of one another now, and haven’t been totally independent in the past (though there once was a lot of isolation by distance)
okay, moving right along…let’s take up definition 2 (the things that speciation gives rise to)

2a. Biological Species Concept (BSC) - a set of actually or  potentially interbreeding populations separated by other such entities by intrinsic reproductive isolating barriers

These barriers can exist at any stage in the life cycle
Prezygotic barriers                   Postzygotic barriers
• adapted to different habitats   • embryos don’t work well
• breed in different seasons      • don’t signal properly to get fed
• female doesn’t recognize male    • feeble
• courtship doesn’t work           • sterile (e.g. meiosis fails)
• genitalia don’t fit well            • do fine but beyond the F1 generation there’s hybrid breakdown due to the disruption of coadapted gene complexes
• sperm and egg incompatibilities  

BSC
a. nice for sympatric organisms, but not so great for allopatric ones
b. note how futuristic the BSC is - hard to know about what is potentially possible (conditions might change in the future)
c. it’s not just “can you breed them in a zoo or garden,” because if they would never meet in nature due to being adapted to different habitats, then they are still independent
d. doesn’t say how separate or how complete; is a little bit of interbreeding okay?  (lots of species hybridize occasionally)
e. lots and lots of cryptic biological species might exist

2b Phylogenetic species concept (PSC) - the smallest group that is monophyletic and diagnosable (Fig. 15.2)
a. you would have to look at a bunch of gene genealogies, since if you look at any one gene, local populations, families and individuals would be monophyletic (assuming no recombination within that gene)
b. diagnosable depends on how hard you look, and even many individuals would have a new mutation somewhere in their genome
c. nevertheless, the PSC is historical, not futuristic, and as such it is about what has happened not what might happen.

There are probably a whole lot of cryptic species out there Taxonomists’ perusal is pretty superficial and might miss a lot of biodiversity (in ecology, physiology, etc.). For example, elephants (Fig. 15.4).

the origin of species can happen in lots of ways, but the most plausible (and probably the most common) scenario is:
• allopatry causing extrinsic isolation
• diversifying selection causing divergence in ecology
• correlated response to selection in reproductive system
(notice that different groups would have different amounts of morphological divergence before reproductive isolating barriers became strong)

Mechanisms of isolation
(1) truly geographic isolation through dispersal or vicariance (Fig. 15.5)
Hawaiian drosophila Fig. 15.7
15.8. snapping shrimp in the Pacific and Caribbean separated by the isthmus of Panama
clade 6 and 7 are deep water groups
others are shallow, separated when the isthmus was complete
(2) instant genetic change that makes a reproductive isolating barrier
    -polyploidy
    -chromosomal change
    -macromutation

Mechanisms of divergence causing reproductive isolation (this is what is called speciation in the strict sense)

• genetic drift (especially relevant are founder effects following a new colonization)
• natural selection
    - unique mutations
    - diversifying selection in allopatry
    - disruptive selection in sympatry (Rhagoletis example)
• sexual selection (especially if female choice is coadapting with male ornaments)

hybridization implicated in the origin of a lot of plants in certain groups (even without polyploidy)
certain groups of animals also hybridize a lot, but maybe it results less often in new successful species
Big Mystery (I think):  how can you have rampant hybridization, as very occasionally does happen, without the two parent species becoming homogenized?
When hybrids are abundant, it is generally in a hybrid zone
Fig. 15.15. sage brush subspecies in which hybrids do best at intermediate elevations

traditionally the problem to explain is how evolution in survival characters causes evolution in reproductive characters (assortative mating) - this is the double variation problem
but speciation is so much easier if one allows for single variation in which selection causes evolution of one set of genes that also affect reproductive isolating barriers, either because reproduction is the target of selection (sexual selection) or because of pleiotropy or possibly because of hitchhiking
consider pea-aphids (Fig. 15.16):  the same genes (or closely linked ones) that increase fitness on one host also cause a preference for that host.

There are lots of studies in which people have tried to get drosophila to speciate in the lab
sometimes works, often it doesn’t
when you do get the evolution of reproductive isolating mechanisms it is usually when you set up very strong diversifying selection on several traits simultaneously
this sometimes works in even in sympatry

another little curiosity…
a number of studies in which people have hybridized plants in the garden and after a few generations they have evolved into new species that were at least partially isolated from the parents
also, in the case of sun flowers:  Helianthus anomalous thought to be from H. annuus x H. petiolaris, but it has some novel features
in the lab this was recreated several generations after crossing with the same linkage groups coming from the respective parents
must mean that there is selection to eliminate other combinations of linkage groups

Mayr’s speciation by revolution
most of the time, species are under stabilizing selection, so they show stasis
bonds of mating keep the species homogenized genes are all working together in a coordinated way, like an orchestra
occasionally colonists break-off from the main population in peripheral populations, in unusual habitats, where founder events
and novel selective pressures force evolution in a few genes
this causes directional selection on other loci that allow for a regaining of balance, which causes selection on yet other loci
there’s a genetic revolution and a reorganization of the genome

so now you have different biological species, but is that the end? …not necessarily ... Secondary contact may cause further evolution

One possibility is reinforcement (or some other form of character displacement)
reinforcement - the species that have become isolated to some partial degree, often in postzygotic barriers, come back together.  There is then selection for prezygotic barriers (species recognition) that save effort from being wasted on hybrids (Fig. 15.13)

Okay, time for some of my lab’s stuff: Looking at Penstemon centranthifolius, Penstemon spectabilis,
and their hybrids…

So we decided to measure the strength of reproductive isolating barriers

We made conspecific crosses (CC x CC, SS x SS)
    backcrosses (CC x F1, SS x F1)
    and heterospecific crosses (CC x SS, SS x CC)

And we measured success at moving through the life cycle
    pollen germination
    pollen tube growth
    fruit set
    seed set
    seed mass
    offspring performance

At each stage of the life cycle we figure out the proportional success of heterospecific crosses compared to conspecific crosses
We then multiply these pure effects through the life cycle to calculate the cummulative effect at any stage

•When P. spectabilis was the maternal parent and F1s were backcrossed to P. spectablis:
Measured Effect    Pure Effect    Cumulative Effect
Pollen adhering, a=0.978    a=0.978    0.978
Tubes at top of style, b=1.043    b/a=1.066    1.043
Tubes at bottom of style, c=0.779    c/b=0.747    0.779
Seeds produced, d=0.457    d/c=0.587    0.457
F1 performance, e=1.030    e=1.030    0.471
F1 sired pollen adhering, f=0.950    f=0.950    0.447
F1 tubes at top, g=0.854    g/f=0.899    0.402
F1 tubes at bottom, h=0.702    h/g=0.822    0.330
F1 sired seeds, i=0.729    i/h=1.038    0.343
Backcross performance, j=0.968    j=0.968    0.332

•When P. centranthifolius was the maternal parent and F1s were backcrossed to P. centranthifolius:
Measured Effect    Pure Effect    Cumulative Effect
Pollen adhering, a=0.700    a=0.700    0.700
Tubes at top of style, b=0.591    b/a=0.845    0.591
Tubes at bottom of style, c=0.593    c/b=1.003    0.593
Seeds produced, d=0.024    d/c=0.041    0.024
F1 performance    —    —
F1 sired pollen adhering, f=0.865    f=0.865    0.021
F1 tubes at top, g=0.879    g/f=1.016    0.025
F1 tubes at bottom, h=0.812    h/g=0.925    0.022
F1 sired seeds, i=0.173    i/h=0.213    0.004
Backcross performance    —    —

And then we had all these hybrid plants, so we wanted to know about the genetic basis for the differences between the species
(which in this case are differences between pollination syndromes). Generally, we found that the hybrids and backcrosses were right in between their parents for many characters. Hummingbirds and bees also more or less treated them as intermediate, although there was an apparent threshhold for how long a hummingbird would stay at a plant.

You can skip Ch. 16, so we’re down to just Ch. 17 & 18, which are part on actual history; part on macroevolutionary processes
• Nature of the fossil record (it’s incomplete)
• Cambrian explosion and the phanerozoic
• Macroevolutionary patterns & processes
    -Radiations & key innovations
    -Punctuation and stasis
    -Mass extinctions and the radiations that follow
• K-T event and “the human meteorite”

punctuated equilibrium - the pattern of species arising relatively quickly (1000s of generations) and then not changing much for a long while.  cf. phyletic anagenesis
Fig. 17. 15. in other words, is evolutionary change mostly around speciation events?

Fig. 17.16. two groups of bryozoans say “YES”
it’s hard to quantify, but an awful lot of species that persist in the fossil record for long periods or are geographically widespread and seem to be morphologically static

what could be responsible for stasis and punctuation?
could be due to Mayr’s genetic homeostasis and speciation through revolution (Eldredge and Gould’s original inspriation)
or could be because of more external (niche) reasons: if niches are fixed and species are being sorted based on where they live best, then they will sort themselves into places where they experience stabilizing selection. This is called habitat tracking (the book’s definition is messed up).

Fig. 17.18. horseshoe-crabs have hardly changed since they appeared 150 Ma, but they have plenty of genetic variance
the group containing the king crab and the hermit crab displays great disparity and has less genetic divergence

The really curious thing about stasis is it seems to be not only at the species level:  phylogenetic conservatism is overwhelming around the level of species but also genera, families, orders, etc.  Also, it’s idiosyncratic - it affects traits of obvious importance and traits we don’t know the function of - it affects different traits in different lineages.  Stasis is the great unexplained truth of biological diversity.

Conservatism could be due to the character being a functional adaptation that is constantly under stabilizing selection directly.
It might come to be canalized whereby the genetic system comes to make the character despite hidden genetic variation.
This could eventually mean that it would remain conservative even with out stabilizing selection on it per se.
Either way, many characters have been imburdened.

Given that some characters seem to get imburdened, this opens up the possibility of hierarchical clade selection in which some
clades are more ‘successful’ than other clades because of their characters

Furthermore, consider Gould’s grand analogy…
microevolution            macroevolution
mutations                conservative adaptations
individual selection            clade selection
genetic drift                clade drift
mutational drive            directional speciation
niches                    adaptive zones
adaptations of (ind’l) organisms    diversification of major groups
life history tradeoffs            speciation/extinction -corr

There are two aspects of being successful:  (1) higher speciation
rates, and/or (2) longer endurance
So, one could have
• an innovation that favors radiation
• an innovation that favors endurance
• an innovation that disfavors radiation
• an innovation that disfavors endurance

clades of insects that have become herbivores are very species-rich compared with their sister clades
so herbivory seems to be an innovation that favors radiation perhaps through coevolutionary forces (like lots of opportunities
to specialize)
actually, plant clades with latex or resin as a defense are also very species-rich compared to their sister clades, so maybe it works both ways

This arrangement would show an innovation that disfavors radiation, perhaps evolving great dispersal ability (bird dispersed fruits)

You could also have innovations that favor endurance; in other words tend to delay extinction

or ones that disfavor endurance like maybe being obligately asexual
in practice it is very hard to tell whether a bias is because of speciation rates or extinction rates

for marine bivalves, having planktotrophic larvae seems to make extinction less likely (Fig. 17.23)

what we’re really talking about here is clade selection, something that is just a bit more general than species selection

the idea is that species have characters that are more or less static and in any given community they are able to colonize and become establish or they go extinct (in part) because of those characteristics

the fixation of adaptations that characterize species (perhaps often originating during punctuations) is analogous to mutation

so when you see an organism is apt to its environment, you don’t know if this is because of mutations + normal individual selection in this environment or because of ancient innovations + species selection

we stumbled upon the processes of community assembly a.k.a. species sorting (sometimes meant to include species drift as well), a.k.a. ecological fitting
particularly relevant to species interactions (pollination, fruit dispersal, competition, parasitism):  the species that we
see associate with each other today, did they coevolve or were they assembled because they didn’t drive each other to extinction?

Something to think about:
Remember that usually when individual selection is pitted against higher level selection (at least in sexual organisms), individual selection gets its way because the episodes of selection are more frequent.
This requires there to be genetic variation for selection to act upon.
Lineage selection (which perhaps only works in very special circumstances) is when selection at the higher level deprives individual selection of genetic variation, e.g., the maintenance of sex.

characters are not the only thing that can affect speciation and extinction rates - also there are circumstances
A plant gets dispersed to a new volcanic island and radiates into 100 species
Dinosaurs go extinct, and rats take over the world
So, innovations, or circumstances, or (very often) the interaction of the two are what determine which clades are diverse and which clades are monotonous

adaptive radiations are groups where there has been great diversification in many different modes of life
a key innovation may move a clade into an adaptive zone - a set of niches that are open to be filled (Fig. 17.13)

these macroevolutionary processes act at scales of the dynamics within a genus (Penstemon) all the way up to the pageant of
the metazoa

Considering the history of the metazoa (Fig. 17.20, 17.21), there have been five really big mass extinctions: end of Ordovician
end of Devonian, end-Permian, end Triassic, and K-T

The K-T event, we’re pretty sure now, was demarcated by a bolite (meteorite) from space, one the size of a mountain
Fig. 17.26. The Chicxulub crater

Fig. 17.27. Excluding rudists, bivalve extinction rates are independent of body size

In other words, the during mass extinctions some rules that are followed by background extinctions no longer hold


Other rules work even during mass extinctions. Fig. 17.28. bivalves with larger ranges were less likely to go extinct.


Short history of the life…
• Starting 3,500,000,000 years ago, bacteria have been abundant
• Then eukaryotes arose, maybe 2,000,000,000 years ago
• Multicellularity traces back to ~600,000,000 years ago
• Animals really got big and fancy during the Cambrian, 543,000,000 … 505,000,000 years ago

Fig. 17.12. A short history of animals (metazoa)
several lines of evidence suggest a very substantial pre-cambrian history
then in 1% of the history of the earth, all the phyla appeared
did they just become big and armored?
maybe a sudden increase in O₂ allowed it to happen

There were other times of great radiations, often in what we call orders, e.g., the orders of mammals in the Paleocene

We divide the Phanerozoic into three great ages:
    -Paleozoic (543-251 Ma), plants, insects, trilobites, etc., ended with the Permian extinction
    -Mezozoic (251-65 Ma), dinosaurs, gymnosperms, ended in the K-T extinction
    -Cenozoic, lots of mammals, angiosperms, etc., still underway

Fig. 2.18

Fig. 18.1. the genes are expressed in different segments
they determine pattern formation (e.g., which segment comes to have wings)
oddly, they are arranged on the chromosome in the same order in which they are expressed
these same genes are used for a similar role in the development of other animals

Fig. 18.3 (note the duplication of the whole thing in verts)

Fig. 18.5. the Hox genes are in the common ancestor of Onychophora and Arthropoda, but they’ve come to determine a more elaborate pattern in insects

Parsimony says that the common ancestor of flies and mice was not all that elaborated and differentiated (it may have had
light sensitive areas but not real eyes, it may have had anterior/posterior zones but not different segments)
…so, it seems that analogous patterns have been built on the same underlying developmental cascade of gene expression
there’s deep homology but not exactly in the phenotype
the rhythm of development pre-dates the songs that were set to it

Now on to flowers…
Remember the common ancestor of animals and plants was unicellular - multicellular development wouldn’t have even made
sense for it
But something vaguely similar arose in animals and plants (deep analogy), homeotic pattern formation genes
In flowers there is a cascade of gene expression determining what will be an inflorescence, what will be a flower, and then the ABC genes determine the flower parts
also many of these genes are found in non-flowering plants
convergent evolution has occurred in the logic of how development is orchestrated

And once a system is established, it shows enormous conservatism
With maybe only a couple exceptions in 250,000 spp. of angiosperms, the order of organs (when present) is carpels, stamens, petals, sepals (Fig. 18.16)
even though one can make mutants to the contrary

heterochrony - changes in the timing of development and maturation
tiger salamander adult (left), larval (below)...axolotl, a paedomorphic species
  -paedomorphosis - the derived condition looks like the juvenile of the ancestor (3 ways to do this: neoteny is when development is slowed down; progenesis is when maturation is sped up; and post-displacement is when the initiation of development is postponed)
  -peramorphosis - the ancestral adults look like juveniles of the descendant developmental series (3 corresponding way to do this: acceleration is when development is sped up; hypermorphisis is when maturation is slowed down; and predisplacement is when development is given a head start).

heterochrony
-could be global or could affect just one organ (the flower, the face)
-often seems to be associated with a change in life history strategy, e.g., from r- to K-strategy
-potential for a lot of morphological/ecological change from a tiny genetic change affecting already coordinated development

actually, almost all changes in morphology are a form of ‘local’ heterochrony
few other possibilities exist: de-novo evolution, which is probably extraordinary, and heterotropy, e.g., changes in the position as in nectaries moving from the petals to the stamens

"Heros" of evolutionary thought

The pre-darwinian scene
Great French Zoologists (generally at each other’s throats):
•Jean Baptiste Pierre Antoine de Monet, Chevalier de Lamarck
•Georges Cuvier
•Etienne Geoffroy Saint-Hilaire

William Paley: Natural Theology. The great functional design of organisms implies a designer.

Charles Lyell: Principles of geology. uniformitarianism, gradualism, the great age of the earth

The Age of Darwin (1859-)
Charles Darwin
-voyage of the Beagle
-corals, barnicles, etc.
-thought out evolution in secret
1859 - The Origin of Species
1881 - The Descent of Man

Alfred Russel Wallace
-figured out the biogeographic origin of species, then natural selction, then wrote about evolution and biogeography for decades more

Thomas Henry Huxley
“Darwin’s Bulldog”
Brilliant essayist and public speaker
Took the idea of evolution and ran with it, for instance writing about how it explains the oddities of anatomy and about how it is no good guide to ethics

The Middle Ages of Evolutionary Biology (1883-1899)
Ernst Haeckel
coined many terms like “ecology”
said (wrongly) that “ontogeny recapitulates phylogeny”
Explored many aspects of evolutionary biology; interested in modularity

August Weismann (1934-1914)
-anti-Lamarckian; strictly selectionist
-articulated the importance of the germ line, had ideas about chromosomes and heredity

Francis Galton (1822-1911)
• Invented regression
• Galton’s polyhedron
(Darwin’s cousin)

Hugo de Vries (1848-1935)
-One of three who rediscovered Mendel
-Before that a loyal student of darwinism
Should have been the intellectual heir, but didn’t quite make it; spoke of ‘genes’
(misled by the crazy inheritance in evening primroses)

The Mendelians versus the Biometricians (1900-1920)
Karl Pearson (1857-1936)
-Involved in inventing many statistics (r, X²)
-Motivated to study evolution by studying variation and parent-offspring inheritance
-Distained evolution by large Mendelian mutations (saltations); the archetypal biometrician

William Bateson
-Seized on the discrete nature of Mendelian alleles; the great hipster of the day but never really got it straight
-Materials for the study of Evolution

Fisher, Wright & Haldane (1920-)
Sir Ronald A. Fisher (1890-1962)
Father of population genetics (evolution on the assumption of Mendelian genetics)
1930 - Genetical Theory of Natural Selection
(Huge contributor to statistics and experimental design; argued for eugenics)

Sewall Wright  (1889-1988)
Pioneer of population genetics
-evolution on the assumption of Mendelian genetics
-genetic drift
-shifting balance theory

J. B. S. Haldane (1892-1964)
-Population Genetics, with many of the classical applications (peppered moths, sickle-cell anemia)
-Popularizer of science (Marxist)
(retired to Hindu mysticism)

Hermann J. Muller
-The production of mutations by irradiation
-Genetic load
-Muller’s ratchet
(Nobel prize)

The Golden Synthesis (1937-1963)
Theodosius Dobzhansky (1900-1975)
1937 - Genetics and the Origin of Species
Reproductive isolating mechanisms
The genetics in natural populations (of fruit flies)

Ernst Mayr (1904-2005)
•1942 - Systematics and the Origin of Species. Presented the biological species concept and the textbook allopatric model of speciation
•1963 - Animal Species and Evolution. The cap-stone of the Synthesis, including a reason for species stasis & peripatric speciation by genetic revolution
• Plus many other books on the history of evolutionary thought and basic biology
Notable as well as an editor and elder statesman of evolutionary biology

George Gaylord Simpson (1902-1984)
Paleontologist, took population genetic thinking and explained macroevolution, also many other ideas about such things as adaptive zones
1944 - Tempo and Mode of Evolution
1953 - The Major Features of Evolution

Sir Julian Huxley (1887-1975)
generally a member of the intelligencia,
interested in ontogeny, theological implications
Editor of The Modern Synthesis
(grandson of T.H. and brother of Aldous)

G. Ledyard Stebbins, Jr (1906-2000)
Brought plants into the Synthesis
1950 - Variation and Evolution in Higher Plants
1974 - Flowering Plants: Evolution above the species level

Jens Clausen, William Heisey, David Keck
1930’s-50’s - Experimental Studies on the Nature of Plant Species

The Age of the Selfish Gene (1964-1980)
John Maynard Smith (1920-2005)
1979 - The Evolution of Sex
1982 - Evolution and the Theory of Games
Many other books before and after. Lucid writer about mathematical ideas in evolution.

William D. Hamilton (1936-2000)
-Kin selection
-Sex ratio evolution
-Sexual selection: effect of parasites
Refined many other of the main ideas of his times
(sad but fitting death from malaria)

George C. Williams
-Evolution of senescence
-Bashing group selection
-Evolution of sex
-Darwinian medicine

Richard Dawkins
Popularizer of evolutionary logic
1975 - The Selfish Gene. And many other books since then
(loathed by creationists, a celebrator of the mechanistic beauty of nature)

Edward O. Wilson
-Island Biogeography
-Sociobiology
-Biophilia
-Ants

Stephen Jay Gould (1941-2002)
• Generally critical of the thinking of the others (especially E. O. Wilson)
• Popular essayist
• Coined “punctuated equilibrium”
• Critiqued “adaptationist program” and coined “expatation”
• Argued for hierarchical (macro-) evolutionary processes
• Parting book: 2002 - The Structure of Evolutionary Thought

Motoo Kimura
1983 - The Neutral Theory of Evolution

The Methodist Reformation (1980-2000)
Joe Felsenstein: comparative method, bootstrapping, maximum likelihood
David Swofford: programmer, wrote PAUP

Rosemary & Peter Grant
-Evolution in action with Galapagos finches
-Rigorously studying evolutionary ecology

What next?
Mary Jane West-Eberhard
-Wasp social evolution
-Speciation by sexual selection
Magnum Opus: 2003 - Developmental Plasticity and Evolution

What is the field of evolutionary biology? It is a thematic perspective centered on logic. It draws off of all the other provinces of biology (and geology) that all have their own subjects and methods (genetics, physiology, ecology, development, systematics, etc.).

Ch. 19. Human evolution
Who are are closest relatives?  {gibbon,{orangatang,{gorilla, {bonobo, common chimp}, human}}}

Humans and chimps diverged ~5 million years ago (remember life got started about 3500 million years ago).
We can trace our history through the bush of life: human characteristics evolved in many stages and with some no-extinct cousins.  Forms included gracile australopithocines, robust australopithocines, Homo habilis, Homo erectus, etc. They often existed simultaneously.  Brain size got bigger gradually.

Human characteristics
-bipedalism
-reduction in hair; more sweating; physiology of long-distance walkers
-very handy; tools very elaborate
-short snouts for eating cooked food
-females sexually interested all the time (not just a few weeks when they need some sperm)
-beautiful breasts (I think)
-language
-huge heads
-long development times
-menapause
-natural-born naturalists, telling stories of snakes and when the world was young; not easily taught quantum mechanics