EVOLUTION – Biology 4250
Review Sheet Number 2 – Test 2
In most cases, you will be responsible for examples of the concepts that are presented in the
text book, as well as the other examples that I present in the classroom.
Chapter 6: Mendelian Genetics in Populations -- Selection
and Mutation as Mechanisms
You should know how to use a Punnett Square to determine potential offspring from a
cross between two parents with specified genotypes.
The Hardy-Weinberg Equilibrium Principle: A review (from Biology 1108)
Populations with no selection (or mutation, genetic drift, etc.) should not evolve, meaning no
change in allelic frequencies from generation to generation. If such populations existed, then
frequencies of both the alleles in the population as well as genotypes of individuals should remained
We will talk about the Numerical example involving "mice" on pages 171 to 177, or some similar
case where we can actually COUNT the alleles in a fictitious population, then apply this to the more
general case of the H-W Equilibrium principle.
The General H-W equation (for a trait with two alleles, one dominant/one recessive):
p = frequency of dominant allele (freq. A) Hopefully it is clear that in this case
q = frequency of recessive allele (freq. a) p + q = 1 (which represents 100%)
Additionally, inserting frequencies into the Punnett Square (see pages 174 & 178),
p2 = frequency of homozygous dominant individuals in the population (freq. AA)
(pq + pq) = 2pq = frequency of heterozygous individuals in the population (freq. Aa)
q2 = frequency of homozygous recessive individuals in the population (freq. aa)
And again, hopefully it is clear that in this population,
p2 + 2pq + q2 = 1 (100% of the individuals in the population)
YOU WILL be expected to reproduce the above equations and to be able to use them to figure
out frequencies in (artificial) populations (a homework assignment is coming up next week).
Are populations in H-W equilibrium, and, if not, what use is the H-W
Clearly, the H-W equilibrium principle has several assumptions:
1. No selection; individuals contribute equally to future generations regardless of phenotype.
2. No mutation.
3. No immigration (followed by mating) or emigration (pop in isolation) -- no GENE FLOW.
4. No chance events that allowed some individuals to mate a lot more, or chance events that
killed individuals of a certain genotype.
5. Mating is random; no mate choice based on mate characteristics.
The point? Clearly, NONE of the above assumptions are likely to be true in any natural population.
So what use is the H-W equation? The H-W equilibrium is, in essence, the NULL hypothesis for
evolution, because if the allelic frequencies are NOT in equilibrium then it means . . . evolution.
And, since the assumptions are clearly not met, then what can we say? EVOLUTION is occurring!
Selection and its effects -- testing assumption #1 of the H-W principle
As we already know, different phenotypes have different fitness, based on how well adapted
individuals are to the current environmental conditions -- remember, fitness has two components:
1) survival to reproductive age and 2) reproduction once reaching reproductive age. The point is that
there are selection pressures (weather conditions, food/water/shelter/mate availability, etc.)
on individuals in the population, and different phenotypes may fair better or worse. It can be complex,
however, since an individual better at getting shelter will not necessarily be better at getting mates.
On pages 183 - 184, selection is added to the mouse example (from earlier) such that one of the
alleles is now somewhat detrimental in the heterozygous individuals, and even moreso in the
homozygous individuals. End result? Decrease in the frequency of that allele by the next generation.
The experimental example of altering AdhS/AdhF allele frequencies over 50 generations in Drosophila
melanogaster (fruit flies) by providing ethanol in the diet of some strains but not in others, is a simple
and elegant example of selection. Other examples (like HIV resistance in humans) are also discussed.
You should be able to CALCULATE allele frequencies from one generation to next when given
simple selection for/against percentages for different genotypes (for traits with two alleles; see pgs.
183-184 and 186-188).
Patterns of Selection
Selection on recessive/dominant alleles -- the Tribolium example, with a recessive lethal allele;
Huntington's chorea, a dominant allele in humans
Which is stronger? Selection in pops with recessive or dominant lethals?
Selection on homozygotes/heterozygotes -- eg., sickle cell heterozygotes in malarial regions
Overdominance -- selective advantage for heterozygotes.
Homozygote advantage over heterozygotes -- eg., Drosophila compound chromosomes
Frequency dependent selection (most often this involves selection for rare morphs) examples:
1. Yellow and purple elderflower orchids (see text pgs. 206 - 207)
2. male mosquito "song" pitch (females mate more frequently with males whose wing beat
frequency is different producing a different pitch in their "buzz"
3. snail shell pattern and "search images" formed by bird predators; search images formed
much more easily for the more common patterns, even if uncommon patterns might stand
out a bit more
The end result of frequency-dependent selection is to maintain variation in populations, as can
overdominance, as indicated above.
Mutation and its effects -- testing assumption #2 of the H-W
We've already spent quite a bit of time talking about how mutations occur, and to an extent the
effect mutation can have on allele frequencies. Clearly, one effect is establishment of completely new
alleles. More often, however, is mutation from one allele to another, resulting in a change in allele
frequencies. Remember, however, that mutation rates will NOT be a potent force in short term changes
in frequencies of alleles in populations. Mutation rates are typically QUITE small, most are somatic
(not passed on) and most are neutral or detrimental (at most eliminating one individual at a time from the
population, if that).
However, mutations can occur that convert a dominant allele to a recessive and vice versa, which,
as long as both alleles are selectively equal, can alter allelic frequencies with "no harm done". From the
example in the book (pgs. 210-212), you will note that there is still little effect, but "little effect" is NOT
the same as "no effect". Still, mutation will never be a major player in the short term, but do not forget
that in the long term, mutation is EVERYTHING, supplying the new genetic material for real change.
Mutation and Selection
So, as we have already discussed, mutation, which by itself would alter frequencies at a snail's pace,
COMBINED with selection, becomes a potent, indeed THE potent, evolutionary force. This is perhaps
most clearly seen in populations of organisms (the example in the book is a strain of E. coli) that cannot
recombine genetic material, i.e., can only reproduce asexually. With mutation, followed by selection, even
asexual strains can be altered through time. Without mutation, only natural clones would be produced and
evolution would grind to a halt.
As mentioned above, however, remember that, in most cases, there will be a mutation-selection
balance. Since most mutations are deleterious, selection tends to eliminate the mutations, not reinforce
Genes with positive selection -- genes in which beneficial
mutations seem more frequent (Chapter 7)
Positive selection strong in genes that code for proteins involved in defense, reproductive conflict
(sperm competition and sperm-egg interactions), and interactions with symbionts (See Table 7.2,
page 260), and some others. WHY does this make sense?
Selection on "Silent" mutations (also Chapter 7)
If silent mutations were truly silent, then we should see EQUAL distribution of various codons that
code for single amino acids. We do NOT see this. We see a significant codon bias for particular
codons over others, especially in highly expressed (more frequently transcribed) genes (See Table
7.3, page 261). How is such selection possible? Why would it happen?
The leading hypothesis is selection on translational efficiency -- some tRNA's more common than
others. This may indeed explain why "silent" mutations do not accumulate as rapidly as mutations
Chapter 7: Mendelian Genetics in Populations: Migration, Genetic Drift and Nonrandom
Mating. The H-W assumptions 3 through 5 (see page 118, chapter 5).
Note: the chapter starts out with a discussion of Greater Prairie Chickens in Illinois, habitat
declining populations, etc. – make sure you read the introduction, as we will come back to a discussion
of the Greater Prairie Chicken in Illinois towards the end of the chapter.
From an evolutionary standpoint migration is the movement of alleles between populations. This
means immigration/emigration of individuals followed by mating by these individuals – in other words,
gene flow from population to population.
Example of Empirical Evidence on influence of migration on allelic frequencies:
Water Snakes on mainland Ontario/Ohio and the islands in between in Lake Erie.
The Water Snake (Nerodia sipedon) varies in pattern from very plain tan (unbanded) to
strongly banded with darker brown. On the mainland, all populations seem to be completely strongly
banded forms; on the islands are lightly banded to unbanded tan forms. Since the snakes have a unique
basking "platform" of limestone along the shores of the islands, it would seem that the unbanded form,
especially in the young, would be much better protected from predation. Indeed, mark-recapture
studies of snakes from juvenile to adult stages directly indicates greater survival rates in the unbanded
forms than any of the banded forms. So, how come there are ANY banded individuals on the islands?
Answer: continued migration from mainland, with subsequent mating (gene flow). A related question:
How come those on the mainland are virtually all strongly banded?? Answer . . . ???
NOTE: Migration is working in opposition to selection on the islands.
In general, gene flow (migration) tends to homogenize populations, making the
more similar to each other (which can offset to an extent the different selective pressures the populations
are experiencing). So, gene flow reduces differences between populations, but can (though doesn’t
necessarily) increase variation within populations by sharing more alleles.
This concept involves any change in allelic frequencies due to chance events; typically these
changes are much more evident when population size is small (as you will see). These chance events
be anything from "sampling error" in selection of gametes to potentially catastrophic events that cause
death of individuals at random. This, in essence, is "blind luck" functioning as a mechanism of evolution.
Mathematical model of drift:
In a hypothetical and very small population of ten mice with a starting freq. of A = 0.6 and freq.
of a = 0.4, selecting gametes at random from the population to produce a new population of ten mice
will result in a filial population in equilibrium with the parental (p = 0.6, q = 0.4) only about 18% of the
time (see Fig. 7.11, pg. 235). Although this is hypothetical, it does show that changes can result solely
as a function of chance events.
Why is population size so important? The in-class "falling rock" example.
The Founder Effect
Where (and/or when) are populations naturally small?
The most likely occurrence of populations that are small is when new populations are being
founded. The founders are a small subset of the parental population, and, by chance, the frequencies of
alleles in the founders can therefore be different from the averages in the parental population. Sometimes,
founders could even be single individuals, such as gravid female arthropods.
The Silvereye (Zosterops lateralis) and the New Zealand Island chain (page 237)
A nice example of a founder effect can be seen in humans. The Amish populations of eastern
Pennsylvania are descended from around 200 individuals in the late 18th century. One of the founders
carried the recessive allele for Ellis – van Creveld syndrome, a rare form of dwarfism (on chromosome 4).
In the general U.S. population, the frequency of this allele is around 0.001, but in the present-day Amish
population it is around 0.07.
With nothing else influencing allelic frequencies (which, of course, rarely if ever
tends to decrease heterozygosity, and fix alleles in the population, though this is not inevitable,
especially in large populations and with other factors influencing allelic frequencies. Still, alleles could
conceivably be fixed by drift, even in somewhat larger populations (SEE pg. 240). This would result in a
loss of variation.
Experimental Evidence for fixation of alleles:
Brown eye alleles and Drosophila melanogaster
Started with allelic frequencies at 0.5.
After 19 generations of 16 flies (eight males, eight females), out of 107 lines, 30 had lost the
brown eye allele completely, 28 others had it fixed at a frequency of 1 (though the overall frequency for
all lines of the brown and "normal" eye alleles for all lines remained close to 0.5) -- as expected, reduced
heterozygosity and approximately half the lines fixed after 19 generations.
So, genetic drift can be an important evolutionary event because:
1. EVERY population experiences drift, which means EVERY population follows its
own unique evolutionary path.
2. Given enough time (without other significant influences, a MAJOR assumption),
drift can produce substantial change, even in fairly large populations.
3. Small populations may be strongly effected by drift in fairly short time periods.
4. Genetic drift tends to reduce variation within populations, though increase
differences between populations. This, of course, would be offset by migration
(and moderated by selection effects).
Genetic Bottlenecks: Examples of Empirical evidence for genetic drift
The Ozarks Collared Lizards – seven distinct fixed genotypes among the populations
(see Fig. 7.18, pg. 246)
Among four species of plants (Fig. 7.19, pg. 248), smaller populations almost
invariably had lower heterozygosity and polymorphism.
Separate breeds of dogs
How quickly can NEW alleles "take over"
(become fixed)? How fast does evolutionary
by drift proceed? New alleles are, of course, produced by mutation. Those that are disadvantageous
may immediately be eliminated (though may reappear through mutation). Some, however, may persist at
very low levels. Neutral mutations, which, of course, include silent (synonymous) mutations, have drift
as a MAJOR influence in their evolution, (see both Fig. 7.21 and Table 7.1, pgs. 253 and 255, respec-
tively) and a new neutral allele may be substituted for another by drift over the course of time. Of course,
a mutated allele with a selective advantage may more rapidly substitute for another.
Fixation of non-selected alleles by "hitchhiking", or selective sweep
-- chromosome number 4
in certain Drosophila species (melanogaster and simulans, page 262-263). No recombination
(crossover) takes place along its entire length, so the entire chromosome is inherited as a single
linked set. Strong selection for one allele on chromosome #4 can "sweep" other alleles around
it to fixation. Indeed, researchers (Berry, et al, 1991) found virtually no polymorphism in a 1.1
kilobase section of chromosome in modest sized samples of these species.
On the flip side, negative selection can reduce frequency of closely linked surrounding alleles
Nonrandom mating, which virtually always indicates some mate selection, probably occurs in
virtually all populations of living organisms. It should be pointed out that nonrandom mating does not
necessarily drive evolution (change allelic frequencies). Nonrandom mating can occur several different
ways: inbreeding, mate choice, which can include true sexual selection. Sexual selection, which will be
covered more fully in chapter 8, can include: 1) directional selection involving one main trait in choice of
mates (will present one example – the peacock tail), 2) frequency-dependent selection of mates (remem-
ber the mosquitos), and 3) multitrait selection of mates. Sexual selection WILL change allelic frequencies,
though inbreeding may not.
In chapter 7, the authors talk some about inbreeding and its effects (the founder effect).
Inbreeding occurs because the breeders involved are a small subset of the overall population.
An Empirical Example – Inbreeding and Inbreeding depression
As suggested above under the genetic drift section, inbreeding will reduce heterozygosity
(increase homozygosity). This, in turn, leads us to the concept of inbreeding depression. Sea Otters
indeed show lower than predicted numbers of heterozygotes in natural populations, if the populations
were mating at random. There are LOTS of examples we can point to, including lots of self-fertilizing
plants, the Cheetahs mentioned above, egg hatch in many birds (see Fig. 7.30, pg. 272), etc. Needless to
say, organisms have evolved mechanisms to avoid inbreeding. Mate choice (with the ability to recognize
close relatives), dispersal (migration) drives, and self-incompatibility (in plants) are all important mechan-
isms for avoiding inbreeding. Still, in small populations, inbreeding may be unavoidable, and this may
present a formidable challenge when trying to save rare and endangered species which, needless to say,
may be represented by one or a few small populations.
So, what does all of this have to do with Greater Prairie Chickens in Illinois? Hopefully, by now,
you’ve figured it out! What DOES all this have to do with Greater Prairie Chickens in Illinois? The answer
is . . . a "mutational meltdown" and a possible "extinction vortex", even in the face of increasing habitat
availability. The solution? Import birds!
Chapter 8: Evolution at Multiple Loci: Linkage and Sex
Start with the model of
selection presented in Chapter 6, the model predicted extremely
course of evolution in flour beetles (Tribolium) over 12 generations (page 196) – a powerful model
under the circumstances. However, it must be pointed out that the conditions under which the flour
beetles were grown were very controlled, and the evolution investigated involved a recessive lethal allele.
As the authors correctly point out, for other alleles under complex environmental conditions the price of
mathematical modeling is oversimplification.
In this chapter, we WILL learn how to apply a model to circumstances looking at two
alleles at the same time. This may seem hopelessly abstract, though there are two payoffs to this approach:
1) this approach can be used to reconstruct history of populations and genes (we will finally delve a bit into
the CCR5-∆32 allele that provides some HIV resistance, where it came from, and why it is at the moment
virtually only found in Europe), and 2) this provides insight into why organisms may use sexual reproduction
(as opposed to asexual).
Evolution at two (or more) loci: Linkage Equilibrium/Disequilibrium
When we investigate two different genes at the same time, needless to say those two genes could be
anywhere on the chromosomes. In this section, we will talk for the moment about genes that are linked.
Linked genes, of course, are passed together to gametes, giving those gametes (and the chromosome)
their respective haplotype.
We will go over the numerical example discussed on page 283. Understand that "g" = the frequency
of whatever follows "g"; "D" = coefficient of linkage disequilibrium; and "r" = the recombination rate (the
crossover frequency between genes). A crucial point about this numerical example is that the two pop-
ulation on the page have equal individual allele frequencies.
Linkage Equilibrium – when alleles of two different genes appear to be inherited independent of
each other; the freq. of any haplotype can be determined by multiplying the frequency of the individual
alleles; in other words, freq. of AB = freq. of A X freq. of B, and so on. With this, the coefficient of
linkage disequilibrium (D = gABgab – gAbgaB) is zero. (Hopefully, it will also be clear that genes on
separate chromosomes will be in "linkage" equilibrium, as they are, of course, NOT linked!)
Linkage Disequilibrium – a nonrandom association between alleles at different loci. This is due
to the genes being physically linked. Disequilibrium can be generated in three different ways: 1) selection
on multilocus genotypes, 2) genetic drift, and 3) population admixture. D will not equal zero if linkage
disquilibrium exists, and for reasons that will become apparent, D can range only between 0.25 and -0.25.
Linkage disequilibrium – possible causes (besides being closely linked).
Continuing with the numerical example from page 283, if we add selection against any individual
having two or more recessive alleles, we end up with the results as shown at the bottom of page 287.
As you can easily see, this population will now be in linkage disequilibrium. In this example, there is
multilocus selection – selection acting on BOTH genes.
In a finite population, a mutation followed by selection can lead to linkage disequilibrium. It is the
mutation (a chance event) happening once (infrequently) that led to the disequilibrium (see Fig. 8.4 and
text on pg. 288).
If you have two populations with different frequencies of haplotypes, if they are then mixed this will
establish new frequencies of haplotypes that can easily be considered in disequilibrium.
Reduction/Elimination of Linkage Disequilibrium
Genetic recombination (crossing over) – indicates why sexual reproduction (meiosis) is an impor-
tant part of this discussion.
A crucial aspect of this is that the more closely (physically) linked the genes are ("r" close to zero),
the more difficult to remove the disequilibrium (see Fig. 8.6). The reduction of linkage disequilibrium has
been demonstrated in the lab (see Fig. 8.7).
Why does this concept matter?
. . . Because if genes are linked, selection for an allele at one locus will INFLUENCE frequencies of
(most/all) alleles that are linked to it. What this means is that if A is linked to B, and there is selection on A,
it can change the frequency of B. So, someone studying JUST the frequency of B/b could get the mistaken
impression that there was selection against B, when in actuality selection against A is reducing the frequency
So, one would EXPECT linkage disequilibrium when there are alleles which have a strong selective
advantage or disadvantage. We see this in human chromosome 6, which contains the HLA gene. However,
in general, observed disequilibrium in genes studied is quite low, suggesting that even for those that are
physically linked, crossing over is frequent enough to bring "D" close to zero. For populations that are
significantly inbred, even genes on separate chromosomes can appear to be in linkage disequilibrium. But
even occasional outbreeding appears to significantly reduce linkage disequilibrium.
A Practical Application -- the CCR5-∆32 allele
This allele is a loss-of-function mutation at the CCR5 locus, such that the virus cannot
enter target cells. Individuals homozygous for the ∆32 allele are protected from sexually
transmitted HIV strains. So . . .
Where did the ∆32 allele come from? Why is it only in European populations (at the
An analysis of chromosome #3 shows that the CCR5-∆32 allele is found almost
exclusively together with the marker GAAT and marker AFMB (two non-coding regions with
no effect on fitness very close to the CCR5 allele) in humans with the HIV immunity. So, this
indicates that a mutation resulting in the ∆32 variant occurred on a chromosome with the
haplotype for the two markers; the end result is that ∆32/GAAT/AFMB is inherited as a unit.
The linkage disequilibrium is breaking down a bit, as crossing over has resulted in other haplo-
types. Estimates of recombination rate (crossing over frequency) and mutation rate originally put
the estimate of the origin of the ∆32 allele at around 700 ya (Stephens, at al, 1998). However,
since that time, it has been shown that the original chromosomal map was a bit flawed, and
the presence of ∆32 in bones of 2900 year old humans in a Lichtenstein cave, suggest the
origin of the mutation was a few thousand years ago.
So, is the allele under selection, or could drift have increased the frequency of the allele to
its current level (somewhere between 10 and 20 percent) in European populations? It turns
out that the most recent research indicates that, although drift over a few thousand years could
have increased the ∆32 allele somewhat, that natural selection HAD to be involved to some
extent. The selective forces at work, however, are not known, and if the mutation has occurred
elsewhere, it has NOT persisted (not been selected for).
There are a couple possibilities as to what the selective pressure may have been:
1. the bubonic plague ("black death") that struck Europe during the 14th century;
definitive results on the plague’s causative bacterium, Yersinia pestis, are not in yet.
2. Smallpox is a possible additional selective force, as the normal CCR5 protein can
be used by the pox virus to enter cells.
Chapter 9: Evolution at Multiple Loci: Quantitative
Selection on Quantitative Traits – Quantitative Genetics
Traits showing continuous variation are called quantitative traits – such traits typically
involve additive affects of many genes, as well as some environmental influence. Two examples
already discussed: height and skin color (in humans). These traits do not exhibit an either/or
phenotype (either you have it or you don’t, which is what you see with traits controlled by a single
gene with two alleles). Quantitative traits tend to show "normal" (or near normal) distributions (with
the associated "bell-shaped" curve).
For these traits it is appropriate to ask: What fraction of the variation in height is due to
in genes, and what fraction to differences in the environment? In other words, we are looking for the
heritability of these quantitative traits.
h2 = Heritability = VG =
P = phenotypic, G = genetic, E = environmental
VP VG + VE
Furthermore, h2 = Heritability = VA =
VA______ A = additive, D = dominance
VP VA + VD + VE
The second equation above represents what is called the narrow sense heritability, and is that
is due ONLY to the effects of additive genes (NOT typical dominant/recessive variation).
The concept of variability being both environmental and genetic is actually quite easily
will do a height plot similar to what is shown on page 334. Figuring out HOW the genetic and environ-
mental interact, and how MUCH is genetic, is more difficult.
Remember, offspring can resemble parents due to similarities of environments as well,
so to truly
"figure out" the heritability, you need make sure that similar environmental influences are excluded from
the analysis – this is none too easy, and certainly not viable for human studies!! However, check out
the Song Sparrow example on page 335; also note the human studies of mono- vs. dizygotic twins.
Survival and Reproductive Success – the components of fitness
Note selection differential (S; difference between means of two populations for some additive
character), selection gradient (slope of line representing fitness in relation to some additive character),
relative fitness components of discussion (on pages 338 – 340). Can do multidimensional analyses
like those in Box 9.4.
In the end, you can simplify the evolutionary response to selection with the following
R = h2S
An example from nature: Alpine Skypilots and Bumblebees (Galen, 1996)
Skypilots from above treeline (tundra) are 12% larger than those at treeline. Previously, Galen
had documented larger skypilots attracted more bumblebees, and those that attracted more bumble-
bees had more seedset. So she asked two questions:
1. Is selection on flower size by bumblebees responsible for larger tundra flowers?
2. If so, how long does it take to generate a 12% difference in size?
First, need to estimate heritability: a scatterplot of offspring flower size to maternal
shows a heritability of around 1, but with significant scatter, suggesting she could only safely conclude
that 20% (.2) of phenotypic variation was due to additive genetic variation (and so the rest of the
variation is due to . . . ?). Second, need to estimate strength of selection differential imposed by
bumblebee pollinators: she found a selection differential S = .74 mm for these flowers (meaning
flowers pollinated by bumbles were on average .74 mm bigger), which results in a S @ 5%, in turn
meaning the plants that win have flowers that are 5% larger than the average of the entire population.
So, again using the conservative 20% estimate from above, the response R = .2 x .05 = .01 (or R =
1 x .05 = .05 if using the high end estimate for heritability). So, that means bumblebees should
promote a 1 (up to 5%) change in average flower size in a population of skypilots moved up to the
tundra in a generation. The explanation for the size difference is that the skypilots at treeline are
pollinated by a variety of pollinators, while those above are only pollinated by bumblebees. If bum-
blebees are excluded, skypilots below treeline set seed, but those above do not.
Modes of selection and the maintenance of Genetic Variation: Finally getting to the "meat"
Directional – examples (several)
Stabilizing – gall example from book is a good one (pgs. 348, Fig. 9.26)
Disruptive – beak sizes in various birds (including Darwin’s finches); mimetic forms
Understand that all three are STILL selection, meaning that low fitness individuals are
and overall mean population fitness increases.
In general, it has been typically assumed that WITHIN populations, directional and
selection are rather common, and disruptive rather rare. However, if that is the case then genetic
variation (at least in some traits) should be significantly reduced/eliminated completely over time. So,
what helps maintain the variation? We’ve answered this partly before, but we’ll add more detail here.
1. Most populations are not in evolutionary equilibrium with their environment in terms of
directional/stabilizing equilibrium. There is a slow, steady supply of new mutations. Besides that,
different traits may be experiencing differential selection, and linked traits may maintain some variation
with differential selection, at least until recombination unites alleles that are both favorable under the
2. In most pops., there is a balance between deleterious mutations and selection. We’ve dis-
cussed previously that, although selection removes deleterious alleles, most will remain at low
frequency (in heterozygotes and through continued mutation). However, since with additive effects
of quantitative traits, any deleterious mutation at any one locus may have a very small influence on
fitness, so that there may be significant variation maintained simply because of the many genes involved
in the trait.
3. Disruptive selection, or other patterns (frequency-dependent selection) may be more common
than generally recognized.
Important take home messages
1. If a trait has high heritability in two different populations and those populations have different
means in the additive traits, this does NOT tell us anything about the CAUSE of the differences in the
traits – the different environments can still cause significant differences, even with a high heritability
(the IQ argument fallacy).
It is, of course, difficult to show this with humans, but examples from other organisms have been
tested. For instance, low- vs. high-elevation populations of Achillea (see page 351). Low-elevation
plants make more stems than high-elevation plants. Completely environmental? Results for other traits
(size) in some plants (yarrow, for instance) show that differences disappear if grown under the same
conditions. However, in THIS case, when both grown under low elevation conditions, low elevation
plants make more stems, yet when both grown under high elevation conditions, high elevation plants
made more stems. This was unanticipated, and showed that each population is superior in its own
environment of origin.
2. Heritability tells us nothing about the role of genes in determining traits that ALL members of a