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Introduction to Biological Anthropology: Notes 7
Population genetics and the modern synthesis
 Copyright Bruce Owen 2008
− We have seen that Mendel’s model explains some variations in certain traits
− and cell and molecular biology show us the mechanisms by which it actually works
− Mendel's model is fine for either-or characteristics like green vs. yellow peas, but what about
the vast number of traits that don't work that way, like height or body proportions?
− dichotomous traits are either-or characteristics; they have only two possibilities, like "blood
clots normally" vs. "has hemophilia"
− by the way, there are also some traits that have more than two possibilities that are still
distinct, like red, white, or pink snapdragon flowers
− these might be called discrete variants, but there is not a commonly used term for this, and
we won't treat it as a separate case
− continuous variation (or continuously variable traits) describes traits that have a range of
variation, rather than distinct types
− like height, beak depth in finches, etc.
− there are many, many continuously variable traits that are interesting and important,
probably a lot more than discrete or dichotomous traits
− Mendel’s model can explain continuously variable traits, too
− dichotomous and continuously variable traits are actually just special cases of the same
model
− The key idea:
− dichotomous traits are controlled by just one pair of alleles (at one locus, say the locus for
pea seed color)
− but continuously varying traits are controlled by many pairs of alleles (many loci), with
each pair partially influencing the trait
− traits that are controlled by multiple pairs of alleles (multiple loci) are called polygenic
traits
− there are also alleles that affect more than one trait, or in other terms, have more than one
effect. These are called pleiotropic alleles. We won't deal with them much here.
− Example: Let's use the beak depth measured on the finches studied by Peter and Rosemary
Grant on Daphne Major in the Galapagos
− Imagine that beak depth is controlled by one locus with codominant alleles
− we could do this example imagining simple dominant and recessive alleles, too, but it
would get slightly more complicated
− say the alleles control the amount of a beak-stimulating hormone
− H+ (more hormone), contributes to deeper beaks
− H- (less hormone), contributes to shallower beaks
− so the possible genotypes are
− H+H+ (deep beak)
− H+H- (intermediate beak)
− there are two ways to get this (H+H-, or H-H+), so there are twice as many of these
− H-H- (shallow beak)
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− This only gives three kinds of beaks, not a continuous distribution
− it works just like any other codominant Mendelian trait
but now, imagine that alleles at another locus also affect beak depth
− say, by controlling the amount of calcium available for beak formation
− C+ leads to deeper beaks
− C- leads to smaller beaks
− so now the genotypes are
− H+H+C+C+: biggest beak
− H+H+C+C-: slightly smaller
− H+H+C-C-: slightly smaller yet
− H+H-C+C+: smaller than the biggest, probably not exactly the same as either of the
other two, either
− since the effect of slightly less calcium is probably not quite the same as the effect of
slightly less of the hormone
− H-H-C+C+: smaller than above, probably not exactly the same as any of the others
− and so on down to H-H-C-C-, which results in the smallest beak
− there are 9 potentially different combinations with just two pairs of alleles
now imagine a third pair that also affects beak depth… there would be 27 (3 x 3 x 3)
different combinations
− a fourth pair would allow for 81 different combinations… and so on
a relatively small number of loci (allele pairs) quickly gives a large number of combinations
− each combination will probably result in a slightly different total effect on the trait
− in theory, there should be a large number of different beak sizes, but still with a distinctly
different size for each combination of alleles
however, each genotype does not always produce exactly the same size of beak
− there will be a range of phenotypes (beak sizes) for each genotype, since the beak size is
also affected somewhat by the bird's environment
− its diet, air temperature, etc.
− so each genotype actually produces a range of beak sizes
− the differences between the average size for each different genotype is probably small
− so the variation in beak depth for each combination of alleles produces intermediate beaks
that fill the gaps between the beak sizes theoretically produced by the different genotypes
it smoothes out what might theoretically a large number of discrete beak depths into a range
of continuous variation in the phenotype
even though the underlying genotypes are still distinct combinations of alleles
Cool result: this explains how matings can usually produce offspring that look "blended" or
intermediate between the parents, but sometimes exceed the parents on certain traits: just like
what we really observe
− both parents will generally have a mix of alleles that affect a given trait, like height
− each will have some alleles that promote taller stature, and others that promote shorter
stature
− the offspring each get a random selection of these alleles from each parent
− usually, the offspring will get some alleles for tallness, some for shortness, and will
come out with a moderate height
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− in fact, since each offspring combines a random sample of the father's alleles and a
random sample of the mother's alleles, most offspring will tend to have a mix of alleles
that is somewhere intermediate between the parents
− this looks like blending inheritance
− but occasionally, just by the luck of the draw, an offspring will happen to get mostly
alleles for tallness, or mostly alleles for shortness
− if an offspring got, say, almost all the father's "tallness" alleles and few of his
"shortness" alleles, and almost all the mother's "tallness" alleles and few of her
"shortness" alleles, the offspring could have a higher percentage of "tallness" alleles
than either parent
− this could produce individuals who have traits that exceed those of their parents
− just as we occasionally see in real offspring
− this interaction of many loci affecting single traits is how Mendelian genetics produces
offspring that
− usually look like blends of most of their parents' traits
− but sometimes have traits that are not intermediate between their parents
− This is an important way in which "new" variants are produced for natural selection to act
on
− they are not new alleles, but rather new combinations of alleles
− they may not even really be new combinations, just combinations that are so unlikely by
chance that they don't happen very often
− of course, there is no guarantee that the next generation of offspring will get the same
combination
− in fact, it is very unlikely
− but if the combination leads to that individual having more offspring, the alleles that
make up the combination will become more common
− the more common those alleles become, the more often this combination will turn up…
− consider the corn breeding experiment again
− selection for high oil content in corn pushed oil content from around 5% to 18% in 80
generations
− this is far too fast to be due to accumulating random mutations (which we’ll cover in a
moment) that happened to increase oil content
− instead, it implies that many loci influence oil content
− the starting plants were probably a mix of heterozygous and homozygous at many loci that
affected oil content
− the experimenters were selecting plants that had more of the desired alleles at the many
different loci
− by making these alleles more common, they were encouraging combinations that were
always possible, but were so unlikely that they were almost never seen
− OK, so where do the really new variants come from - not new combinations of alleles, but new
alleles themselves?
− changes in the genetic code
− usually in the sequence of nucleotide bases in a stretch of DNA
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− occasionally in gain or loss of parts of chromosomes, or entire chromosomes
− called mutations
− mutations are generally random
− like randomly replacing a part in a complex machine with a different part
− or randomly removing or adding some parts
if a mutation occurs in a normal body cell, it usually has little impact
− if the mutation does not cause a serious problem for the cell's survival, the cell will go on
dividing normally (by mitosis)
− eventually resulting in a small number of cells of that same kind of tissue in that part of
the body that "inherit" the mutation
− if the mutation causes the cell to grow and divide wildly - as in a cancer - then the
disorderly, aberrant growth of tissue may be harmful to the whole organism, even kill it
− either way, a mutation in a body cell never gets into any offspring, so it cannot affect
future generations, and it has effectively no impact on the evolution of the population of
organisms
but mutations in the cells that produce gametes are important
− because the mutation may be copied into a gamete, which may end up producing an
offspring
− every single cell in the offspring will then carry the new, mutated bit of DNA
− and it might get passed onto the next generation, too
mutations may be caused by many things
− radiation, like X-rays
− this is why doctors may X-ray your torso, but they put a lead shield over your testes or
ovaries
− an occasional mutation in an irradiated body cell is no big deal, but a mutation in a cell
that eventually produces a gamete might be catastrophic for a future offspring
− some chemicals may cause mutations
− errors in the replication of DNA
probably the most common kind of mutations are those in which a single nucleotide base
gets copied incorrectly
− this is called a point mutation
− usually, changing one base out of the three in a codon results in a codon that calls for a
different amino acid at that point in the sequence
− occasionally, changing one base will have no effect at all
− because some amino acids are coded for by several different codons
− changing the last base of GCT, which codes for alanine, to C results in a different codon
at that spot: GCC
− But it just happens that GCC also codes for alanine, so this change would have no
effect on the protein.
if one amino acid is changed
− this may have no effect on the resulting protein
− or may change its shape and function in minor or important ways
most changes are neutral or harmful to the function of the protein
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− just changing something at random in a complex chemical process is not likely to make it
better!
many mutations occur in the vast stretches of "junk" DNA that apparently are never used to
make proteins
− these mutations presumably have no effect on the organism
− they are neutral
there are also larger-scale mutations
− longer stretches of DNA may get removed, duplicated, moved from one region of DNA to
another, or even inverted end-for-end
so new alleles, helpful, neutral, and harmful, are constantly but slowly being added to the
genes in the population (the "gene pool") by mutation
− if one of these new alleles is dominant, it is expressed immediately
− so selection can favor it or weed it out
− but if a new allele is recessive, it is not expressed
− it just lurks, hidden in heterozygous carriers, until two carriers happen to mate and
happen to produce a homozygous offspring (just a 25% chance for each offspring)
− or, if it is codominant or affects a polygenic trait, then it might just add its small effect on
some trait that is also affected by other alleles
− the new and old alleles get shuffled around and recombined
and then the individuals who carry them may be selected against, or may be favored, either
weeding the new allele out of the population or helping to make it more common
Mutations are rare
− the chance of any given portion experiencing a mutation is very low
− but there is such a vast amount of DNA in every cell that the odds of a mutation occurring
somewhere in the functional portion the DNA are actually fairly high
− most gametes probably carry at least one mutation in an allele (that is, not in junk DNA)
− any given individual is likely to have gotten at least one mutation in the DNA from his or
her parents' gametes
− most are probably neutral
− those that are not neutral most often will interfere with the proper function of a protein
− recall that this kind of allele is usually recessive
− because the other copy of the gene is likely to be the normal allele, so the individual still
produces the normal protein
− so the harmful mutation hides invisibly in the organism
− so new alleles are constantly being added to the population
− mostly neutral mutations
− those that are harmful are mostly recessive
− because a mutation most often results in a “defective” protein that does not perform
its expected function
− these harmful recessives are mostly hidden in heterozygous carriers
− because each one is so rare, most probably never meet with another gamete with the
same damaged allele
− so most harmful recessive alleles are rarely, or never, actually expressed
− occasional dominant mutations
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− but these can’t be too harmful
− if a dominant mutation causes the individual to die or not reproduce, it is immediately
removed from the population
− and very rarely, new mutated alleles with beneficial results
− Mutation provides the new alleles, while reshuffling of the alleles provides a huge number of
possible combinations - both are crucial to maintaining variation
− the nature vs. nurture question
− we have been talking as though the main influence on phenotypes was the genotype
− But what about the conditions in which the organism develops and lives?
− "Nature": inherited genes
− "Nurture": environment
− the "nature versus nurture" question is: which is the main determinant of how individuals
turn out (their phenotype)?
− Answer: both, because they are inseparable; you can't have one without the other
− Each individual's phenotype is the result of the interaction of both genes and environment
− You can't have a phenotype without genes, and you also can't have a phenotype that did
not develop in some environment
− both are necessarily part of the process
− So far, we have been looking at inheritance at the individual level
− asking questions like, given parents of such-and-such genotypes or phenotypes, what will
their offspring be like?
− But remember that evolution is about changes in populations, not individuals
− like a certain color of moth becoming more common in the population
− or the average beak depth of all the birds in the population changing over generations
− so, to understand evolution, we have to look at inheritance in a lot of individuals at once
− we usually think of species in terms of what is typical for individuals of that species
− we think of the Platonic ideal, or "form", of a species: the ideal or typical example
− like: "a human is a two-legged, mostly hairless creature with harmless little teeth"
− of course, some humans have only one leg, or none, and yet they are still humans
− this point of view glosses over the variation between individuals
− in the population point of view, we think of species or groups of organisms in terms of the
frequency of traits throughout the population
− population (or breeding population) = a group of individuals that mate mostly with others
in the same group, and little with outsiders
− in reality, populations usually have fuzzy boundaries
− individuals migrate into and out of groups
− individuals mate with others from outside the group
− but the breeding population concept is a useful first approximation
− a population view of a species is in terms of how common certain traits are in that
population
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− like: “a human is a member of a population among whom two-leggedness, mostly hairless
bodies, and small canines are each found in 99% of the individuals”
in terms of phenotypes, we might say "91% of the population has free earlobes and 9% have
attached earlobes"
in terms of genotypes: “49% are FF, 42% are Ff, and 9% are ff”
or in terms of alleles: “70% of the earlobe alleles are F, and 30% are f”
we can think of a population as a gene pool:
− the collection of alleles, lurking in individuals, from which alleles are randomly drawn to
create gametes, which in turn randomly combine to form the next generation of offspring
population genetics: the quantitative study of the frequency and distribution of alleles,
genotypes, and phenotypes in populations
− This allows us to make a more precise definition of evolution, in population terms:
− recall our "preliminary definition" from an earlier class:
− PRELIMINARY DEFINITION: Evolution = change in the frequency or magnitude of
heritable features of a population from one generation to the next.
− this was, sensibly enough, focused on changes in phenotypes, which are what we can directly
observe. Now we can do better:
− Evolution = change in allele frequencies in a population from one generation to the next
− Why focus on alleles frequencies?
− because when the next generation of zygotes is created, allele frequency controls genotype
frequency
− genotype frequency (and environment) in turn controls phenotype frequency
− and phenotypes are what affect natural selection
− When zygotes are created,
− the frequency of each combination (genotype) is determined solely by
− the frequency of the alleles in the gene pool
− and the laws of probability
− so zygotes are created with predictable proportions of genotypes
− then natural selection starts weeding some out
− we can illustrate this by using a Punnett square in a new way
− so far, we have used Punnett squares to represent the mating of a single pair of parents
− but we can also use them to represent all the matings of a whole population
− instead of representing a particular father, we describe the likelihood of any father
producing a certain kind of gamete
− instead of a particular mother, we show the likelihood that any mother’s gamete will be of
a given kind
− for example, say there are two alleles for the thumb joint trait, and they are equally common
(exactly 50% are H and 50% are h)
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Father's gametes:
Father's gametes:
.50 H
.50 h
Mother's gametes:
HH (straight):
Hh (straight):
.50 H
.50 x .50 = .25
.50 x .50 = .25
Mother's gametes:
hH (straight):
hh (hitchhiker's):
.50 h
.50 x .50 = .25
.50 x .50 = .25
− HH and Hh result in straight thumbs
− hh results in "hitchhiker's thumb"
− so 50% of all males' gametes have the H allele, and the other 50% have the h allele
− same for the females' gametes
− so the chances of an offspring getting, for example, a h from the mother is 50%
− of those that got a h from the mother, 50% will also get a h from the father
− so 50% of 50%, or 25%, (.5 x .5 = .25) will be hh (have hitchhiker's thumbs)
− and the remaining 75% will be Hh, hH, or HH
− they all have straight thumbs
− now say that one allele is very common, for example, 90% of all the alleles are h and only
10% are H
Father's gametes:
Father's gametes:
.10 H
.90 h
Mother's gametes:
HH (straight):
Hh (straight):
.10 H
.10 x .10 = .01
.10 x .90 = .09
Mother's gametes:
hH (straight):
hh (hitchhiker's):
.90 h
.10 x .90 = .09
.90 x .90 = .81
− now, 90% of the males' gametes have the h allele, and only 10% have the H allele
− same for the females' gametes
− so the chance of an offspring getting a h from the father and a h from the mother are
− .90 x .90 = .81; 81% are hh (have hitchhiker's thumb)
− note that this is the recessive trait, but 81% of the population express it, because the
allele is so common
− that is, a recessive trait may be common (or it may be rare)
− dominance and recessiveness are completely independent of allele frequency
− there will be a few heterozygotes, since occasionally one parent will have the rare allele
− 10% x 90% = 9% will by Hh, getting the H from the father
− 90% x 10% = 9% will be hH, getting the H from the mother
− adding these together, 18% will be heterozygous, with straight thumbs
− and there will be very few homozygotes for the rare allele, since the odds of two people
with the rare allele mating are low
− 10% x 10% =1% will be HH, homozygous straight thumbs
− in total, 18% + 1% = 19% will have straight thumbs (Hh, hH, or HH).
− we can generalize this relationship between allele frequencies and genotype frequencies using
a concept known as Hardy-Weinberg equilibrium
− the idea is that, given certain assumptions, every allele is equally likely to get into an
offspring as every other allele
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− the assumptions of Hardy-Weinberg equilibrium are:
− 1. no new alleles are introduced (no mutation occurs)
− 2. all individuals are equally likely to survive and mate (no selection occurs)
− 3. the allele frequencies are not changed by individuals moving into or out of the
population (there is no gene flow)
− 4. there is no genetic drift: changes in allele frequency due to chance
− that is, we ignore the possibility of getting very unlikely outcomes
− such as just happening to coin-flip 100 heads in a row
− or happening to produce zygotes in significantly different proportions from the
prediction just due to luck
− this is reasonable if the population is large
− out of 4 coin flips, getting all heads is not too unlikely
− out of 1000 coin flips, it is very unlikely that you will get far from 50% heads
− 5. mating is random
− if the assumptions are met
− then the alleles of all the parents in the population will be randomly distributed in the next
generation of zygotes
− the only thing that affects the proportions of genotypes and phenotypes are allele
frequencies and the laws of chance
− if the assumptions are met, the Hardy-Weinberg equilibrium model says that
− if the frequency of, say, the F allele is called p
− and the frequency of the f allele is called q
Father's gametes:
Father's gametes:
Frequency of F = p
Frequency of f = q
Mother's gametes:
FF (free):
Ff (free):
Frequency of F = p
pxp
pxq
Mother's gametes:
fF (free):
ff (attached):
Frequency of f = q
qxp
qxq
− the frequency of the FF genotype should be p2
− the frequency of the Ff genotype should be 2pq
− the frequency of the ff genotype should be q2
− for example, using the earlobe alleles in a hypothetical population
− say that 70% of all the earlobe alleles are the dominant, free allele (F)
− p=.70
− 30% of the alleles are the recessive, attached allele (f)
− q=.30
− since there are only two alleles, the two frequencies have to add up to 100%, or 1
− 70% + 30% = 100%
− .70 + .30 = 1.00
− say that individuals in this population mate at random, producing many offspring
− what fraction of the offspring will have the each genotype?
− Frequency of FF = p2 = .702 = .49
− Frequency of Ff = 2pq = 2 x .70 x .30 = .42
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− Frequency of ff = q2 = .302 = .09
− Hardy-Weinberg equilibrium implies that, if the assumptions are met, then allele frequencies
and genotype frequencies will continue unchanged, generation after generation
− nothing makes dominant alleles become more common
− nor recessive alleles become less common just because they are recessive
− every generation, the alleles just get remixed
− each time recreating the genotypes in the proportions required by their frequencies and
chance: p2, 2pq, and q2
− allele frequencies only change (that is, evolution only happens) when the assumptions of
Hardy-Weinberg equilibrium are not all met
− the conditions that violate the assumptions of Hardy-Weinberg equilibrium are the opposites of
those assumptions. These are the "forces" that can cause evolution:
− 1. mutation
− changes allele frequencies by introducing new alleles
− 2. natural or artificial selection
− changes allele frequencies in the next generation by causing individuals with some
genotypes to leave more offspring, and those with other genotypes to leave fewer
− 3. gene flow
− changes allele frequencies by removing alleles or adding alleles to the gene pool as
individuals leave or join the population
− 4. genetic drift
− changes allele frequencies in the next generation by chance
− what about non-random mating?
− this changes genotype frequencies, but not allele frequencies
− so it is not, in itself, a cause of evolution
− Gene flow
− individuals move into or out of the population, bringing their different allele frequencies
with them
− or individuals mate with others from outside the population, bringing in the different allele
frequencies of the outsiders in the form of gametes that contribute to the offspring in the
next generation of the population
− definitely happens, but mixing gene pools can’t lead to speciation or anagenesis in itself
− and that is what we are usually interested in
− Genetic drift
− chance variations in allele frequencies
− Say a population has 50% H and 50% h alleles
− we predict 25% HH, 50% Hh, and 25% hh offspring
− in a large population, we can be confident of this
− just as you can predict around 50% heads if you flip a coin 1000 times
− but in a tiny population, by sheer bad luck, the actual offspring might differ from the
prediction significantly
− maybe they produce just 3 HH and 1 Hh offspring
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− now the H allele is much more common in this generation
− the change is long-term: all future generations are derived from this gene pool
− Mutations are crucial, because they create new variants
− but the process is extremely slow
− every human is thought to carry an average of about one new mutation among his or her
roughly 50,000 loci (100,000 alleles).
− so any given locus is likely to get a new variant by mutation in 1 out of 50,000 births
− in a population of 1000 humans, that is one new allele for that locus every 50 generations
− with 20-year generations, that is one new altered allele added every 1000 years
− and the odds of it being the same alteration as any previous one are miniscule
− it would take a very long time for mutation by itself to add a significant number of any
particular new allele to the population
− yet many loci in humans are polymorphic
− polymorphic = having more than one allele
− actually, having more than one allele with a frequency of at least 1% (.01)
− mutation is too slow to randomly build up enough of a given allele to reach 1% of even a
tiny population
− if a locus is polymorphic, we have to assume that something has caused the alternative
alleles to become common
− each was originally created by a mutation
− but mutation simply cannot create a lot of copies of an allele all by itself in any reasonable
period of time
− it could only become more common if something increased the number of copies of it in
the population
− selection
− or genetic drift
− Selection (natural and otherwise) could increase the frequency of a new allele
− Say a newly mutated allele is beneficial
− maybe individuals who have one copy have more offspring
− then it will become more common
− directional selection for or against a trait should eventually eliminate the less advantageous
allele
− yet we see that many loci are actually polymorphic
− why hasn't selection eliminated one or the other allele?
− one reason: heterozygote advantage
− the heterozygotes leave the most offsping
− neither allele is eliminated, because the individuals that reproduce the most have one of
each allele
− example: sickle cell anemia
− there are two common codominant alleles for hemoglobin (a blood protein), A and S
− AA individuals have normal hemoglobin
− in an environment with malaria, some AA individuals die from malaria before
reproducing
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− AS individuals are like AA individuals, except that when an AS blood cell is infected by
the malaria bacterium, it tends to rupture, killing the bacteria and preventing their spread
− in an environment with malaria, AS individuals rarely die from the disease
− SS individuals have "sickling" hemoglobin
− when the individual demands a lot of oxygen from the blood due to exertion or stress,
the blood cells deform into a "sickle" shape, clogging up capillaries and causing a
"sickling crisis" that may be fatal
− SS individuals often die before reproducing
− what happens is:
− each generation, most SS individuals die from sickling crises before reproducing, taking
their S alleles out of the gene pool
− each generation, some AA individuals die from malaria, taking their A alleles out of the
gene pool
− each generation, most of the AS individuals survive and reproduce
− they pass both A and S alleles to their offspring
− this produces more SS individuals every generation, who die
− and more AA individuals, many of whom die
− and more AS individuals, who survive and reproduce
− since the heterozygous AS individuals keep replenishing both alleles in the gene pool,
neither one gets selected away
− even though this ensures that there will be SS and AA individuals produced every
generation
− eventually, the population reaches a balance, where the high cost of S alleles is balanced
against the lower cost of A alleles
− both remain in the population; neither gets eliminated by selection
− this is called balancing selection, which leads to a balanced polymorphism
− neither allele is getting more or less common
− imagine that this population moved to a place where there was no malaria
− now the AA individuals survive just as well as the AS individuals
− now simple directional selection weeds out SS individuals
− the frequency of the S allele drops to a low value
− a low frequency of S alleles remains "hidden" from selection in the occasional AS
carriers
− they don’t suffer any harm themselves
− and since they are rare, they almost never happen to mate with another AS individual,
so they run almost no risk of losing any offspring, either
− now imagine that this population moved back to the malarial zone
− AA individuals would start dying off again
− the rare AS individuals would survive and reproduce best
− the frequency of the S allele would start to rise again
− eventually coming to a balance, determined by the relative costs and benefits of the
three genotypes in that particular environment