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Natural Selection
DNA encodes information that interacts with
the environment to influence phenotype
Among The Traits That Can Be Influenced By
Genetically Determined Responses to the
Environment Are:
1. The Viability in the Environment
2. Given Alive, the Mating Success in the
Environment
3. Given Alive and Mated, Fertility or
Fecundity in the Environment.
Viability
Hb- Locus In
Africa:
Non-Malarial
Area
Viability:
A/A
No Anemia
High
Not Resistant
Malarial Area
to Malaria
Viability:
Low
A/S
S/S
No Anemia Anemia
High
Low
Resistant
Anemia
High
Low
Mating Success
Normal
Diet
Low
Phenylalanine
Diet
p/p fetus develops in
Low Phenylalanine in
utereo Environment
p/p Baby
Born With
Normal Brain
Mentally Retarded
Institutionalized
Low Chance of
Mating
Normal
Intelligence
High Chance of
Mating
Fecundity/Fertility
H/+ In A
Society
With No
Birth
Control,
No
Genetic
Literacy,
and Low
Expected
Lifespan:
Normal
Fecundity
H/+ In A
Society
With Birth
Control,
Genetic
Literacy,
and High
Expected
Lifespan:
Low
Fecundity
Why Are Viability, Mating
Success, and Fecundity/Fertility
Important Phenotypes in
Evolution?
Because All Of These Phenotypes
Influence The Chances For
Successful DNA Replication
Physical Basis of Evolution
• DNA can replicate
• DNA can mutate and recombine
• DNA encodes information that
interacts with the environment to
influence phenotype
Physical Basis of Evolution
• DNA can replicate
• DNA can mutate and recombine
• DNA encodes information that
interacts with the environment to
influence phenotype
Viability
Mating Success
Fecundity/Fertility
Physical Basis of Evolution
• DNA can replicate
• DNA can mutate and recombine
• DNA encodes information that
interacts with the environment to
influence phenotype
Viability
Mating Success
Fecundity/Fertility
These Are Combined Into A Single
Phenotype of Reproductive Success
Or FITNESS
DNA can mutate
and recombine
DNA can replicate
Genotypic Variation
In Demes and Species
Heritable
Variation
In Fitness
Phenotypic
Variation
In Fitness
Environment
Natural Selection Is Heritable
Variation In Fitness
That Is, The Genes Borne By A
Gamete Influence The
Probability of That Gamete
Being Passed On To The Next
Generation.
THINK LIKE A GAMETE!
NATURAL SELECTION IS NOT CIRCULAR
DNA can mutate
and recombine
DNA can replicate
Genotypic Variation
In Demes and Species
Heritable
Variation
In Fitness
Phenotypic
Variation
In Fitness
It’s the
Environment, stupid!
Natural Selection At A Single Locus in A Randomly Mating Deme
Zygotic Frequencies
Environment
Viabilities
Adult Frequencies 
Environment
Mating Prob.
Mated Adult Frequencies 
Environment
Ave. No. Offspring
Mated Adult Frequencies
Weighted By No. of Off. 
AA
p2
Aa
2pq
aa
q2
VAA
VAa
Vaa
AA
p2 VAA
Aa
2pqVAa
aa
q2 Vaa
CAA
CAa
Caa
AA
p2 VAACAA
bAA
AA
p2 VAACAAbAA
Aa
2pqVAaCAa
bAa
Aa
2pqVAaCAabAa
aa
q2 VaaCaa
baa
aa
q2 VaaCaabaa
Let WAA = VAACAAbAA; WAa = VAaCAabAa; Waa = VaaCaabaa
AA
p2
Zygotic Frequencies
Environment
Fitness
Mated Adult Frequencies
Weighted By No. of Off. 
Aa
2pq
aa
q2
WAA
WAa
Waa
AA
p2 WAA
Aa
2pqWAa
aa
q2 Waa
AA
Aa
2pqWAa/W
aa
q2Waa/W
Convert to Freq. By Dividing by
 = W = p2WAA+2pqWAa+q2Waa
Mated Adult Frequencies
Meiosis
Gene Pool
p2 WAA/W
1
1/
2
1/
1
2
A
a
p’= p2 WAA/W + pqWAa/W
q’= q2 Waa/W + pqWAa/W
Gene Pool
A
a
p’= p2 WAA/W + pqWAa/W
q’= q2 Waa/W + pqWAa/W
p’= p2 WAA/W + pqWAa/W
=( p2 WAA+ pqWAa)/W
p’ = p(pWAA+ qWAa)/W
Does Evolution Occur?
p = p’ - p
= p(pWAA+ qWAa)/W - p
= p[pWAA+ qWAa)/W - 1]
p = p[pWAA+ qWAa- W]/W
Does Evolution Occur?
Note, W = W(p+q)=pW+qW
p = p[pWAA+ qWAa- W]/W
=p[p(WAA-W)+ q(WAa-W)]/W
Since p and W are always > 0,
This is the only part of the equation
That Can Change Sign and Hence
Determine the Direction of Evolution
Under Natural Selection.
Does Evolution Occur?
What is:
p(WAA-W)+ q(WAa-W)?
Mean Phenotype of Fitness
Does Evolution Occur?
What is:
p(WAA-W)+ q(WAa-W)?
Genotypic Deviations for the
Phenotype of Fitness
Does Evolution Occur?
What is:
p(WAA-W)+ q(WAa-W)?
This is the Average Excess of the A Allele
for the Phenotype of Fitness
Does Evolution Occur?
p = paA/W
Does Evolution Occur?
p = paA/W
Natural Selection is An Evolutionary Force
Whenever p ≠ 0 or p ≠ 1 (that is, there is
Genetic variation) and when aA ≠ 0 (that is,
When there is heritable variation in the
Phenotype of fitness).
To Understand Natural Selection
THINK LIKE A GAMETE!
Sickle Cell Anemia In Africa
An Example of Natural Selection
The Sickle Cell
Mutation
Infection of a
Red Blood Cell
By a Malarial
Parasite
• Sickle-Cells Are Filtered Out
Preferentially by the Spleen
• Malaria Infected Cells Are Often Filtered
Out Because of Sickling Before the
Parasite Can Complete Its Life Cycle
• The Sickle Cell Allele is Therefore an
Autosomal, Dominant Allele for Malarial
Resistance.
The Sickle
Cell Anemia
Phenotype
Most Deaths Due to Sickle Cell Anemia
and Due to Malaria Occur Before
Adulthood. Viability Is The Phenotype
of Living To Adulthood
• In a non-Malarial Environment, The S Allele is a
Recessive Allele For Viability Because Only the
Homozygotes Get Sickle Cell Anemia.
• In a Malarial Environment, The S Allele is an
Overdominant Allele For Viability Because Only
the Heterozygotes Are Resistant to Malaria And
Do Not Get Sickle Cell Anemia.
Two Complications to This
Simple Story in Africa:
1. Epidemic Malaria is Recent to Most of
Wet, Tropical Africa and the Process of
Adaptation to Malaria in Africa Is Still
Not in Equilibrium.
2. There is a Third Allele, Hemoglobin C,
Involved in the Adaptation to Malaria in
Africa.
Epidemic Malaria in Africa
I CE
LAND
MA
DAGASCA
R
About 2000 years ago, A
Malayo-Indonesian
Colony Was Established
on Madagasgar
Epidemic Malaria in Africa
This Colony
Introduced The
Malaysian
Agricultural
Complex into This
Region
Epidemic Malaria in Africa
This Agricultural
Complex Was Taken
Up By BantuSpeaking Peoples,
Followed by A Large
Expansion of the
Bantu In Africa
About 1500 years
Ago.
The Malaysian Agricultural
Complex In Africa
• Is associated with slash-and-burn
agriculture: Provides habitat and breeding
sites for Anopheles gambiae, the primary
mosquito vector for falciparum malaria.
• Results in the high local densities of human
populations that are necessary to establish
and maintain malaria as a common disease.
Epidemic Malaria in Africa
The Hemoglobin C Mutation
Hb-S
Hb-A
GTG
GAG
Valine
Glutamic Acid
Hb-C
6th Codon
AAG
Lysine
The Hemoglobin C Mutation
Hb-C Is A “Recessive”
Allele for Malarial
Resistance
Hb-A, S and C
Genotypes AA AS
Anemia
SS
AC
CS
Yes
Yes
No No
No
(Severe)
(Mild)
CC
NO
Malarial
No Yes
Resistance
Yes
No
Yes
Yes
Viability
No Malaria
0.2
1
0.7
1
1
1
Hb-A, S and C
Genotypes AA AS
Anemia
SS
AC
CS
Yes
Yes
No No
No
(Severe)
(Mild)
CC
NO
Malarial
No Yes
Resistance
Yes
No
Yes
Yes
Viability
No Malaria
0.2
1
0.7
1
1
1
The A and S Alleles Define An Autosomal Recessive Genetic
Disease: Selection Will Insure it is Rare But Difficult to
Eliminate in a Random Mating Population.
Hb-A, S and C
Genotypes AA AS
Anemia
SS
AC
CS
Yes
Yes
No No
No
(Severe)
(Mild)
CC
NO
Malarial
No Yes
Resistance
Yes
No
Yes
Yes
Viability
No Malaria
0.2
1
0.7
1
1
1
The A and C Alleles Define A Set of Neutral Alleles in a
Non-malarial Environment: Their Frequencies Are
Determined by Genetic Drift and Mutation.
Hb-A, S and C
Genotypes AA AS
Anemia
SS
AC
CS
Yes
Yes
No No
No
(Severe)
(Mild)
CC
NO
Malarial
No Yes
Resistance
Yes
No
Yes
Yes
Viability
No Malaria
1
1
0.2
1
0.7
1
Viability
Malaria
0.9
1
0.2
0.9
0.7
1.3
Observed Relative Viabilities In Western Tropical Africa
Hb-A, S and C
• CC is the Fittest Genotype By Far
• If Natural Selection is “Survival of the
Fittest”, Then Natural Selection Should
Increase the Frequency of the C allele and
the CC Genotype.
• Contrary to Rumor, Natural Selection is Not
“Survival of the Fittest.”
• Natural Selection Is Heritable Variation
in Fitness, so Think Like A Gamete:
Which Gamete Has the Highest Average
Excess of Fitness?
Initial Gene Pool Before Malaria
pS=.005 pC=.005
A
pA = 0.99
Initial Ave. Fitness After Transition
to Malaysian Agricultural Complex
pS=.005 pC=.005
A
pA = 0.99
Under Random Mating, the
Mean Phenotype = W = 0.901
Initial Phenotypes After Transition to
Malaysian Agricultural Complex
pS=.005 pC=.005
A
pA = 0.99
Genotypes
AA
AS
SS
AC
CS
CC
Viability Malaria
0.9
1
0.2
0.9
0.7
1.3
Genotypic Deviation
-.001 .099 -.701 -.001 -.201 .399
(W = 0.901)
Initial Phenotypes After Transition to
Malaysian Agricultural Complex
Genotypes
AA
AS
SS
AC
CS
CC
Viability Malaria
0.9
1
0.2
0.9
0.7
1.3
Genotypic Deviation
-.001 .099 -.701 -.001 -.201 .399
(W = 0.901)
aA = -0.0005
aS = 0.0935
aC = 0.0000
Initial Phenotypes After Transition to
Malaysian Agricultural Complex
aA = -0.0005
aS = 0.0935
aC = 0.0000
The Initial Adaptive
Response To A Malarial
Environment Mediated
By Natural Selection Is
To Decrease A, Increase
S, and Leave C The Same
px = px(ax)/W)
Gene Pool After Several
Generations of Selection Under A
Malarial Environment
A
pA = 0.95
W = 0.907
S
pS = 0.045
pC = 0.005
Gene Pool After Several
Generations of Selection Under A
Malarial Environment pC=.005
A
pA = 0.95
S
.045
Genotypes
AA
AS
SS
AC
CS
CC
Viability Malaria
0.9
1
0.2
0.9
0.7
1.3
Genotypic Deviation
-.007 .093 -.707 -.007 -.207 .393
(W = 0.907)
Gene Pool After Several
Generations of Selection Under A
Malarial Environment
aA = -0.003
aS = 0.055
aC = -0.014
After the Initial Adaptive
Response To A Malarial
Environment, Natural
Selection Continues to
Decrease A, Increase S,
but Now It Also
Decreases C Because aC=
-0.014.
Gene Pool After Several
Generations of Selection Under A
pC  0
Malarial Environment
A
pA 1-pS
Genotypes
Viability Malaria
S
pS
AA AS SS AC CS CC
0.9
1
0.2 0.9 0.7 1.3
As pS increases in frequency, W increases and these
Genotypic Deviations Become Increasingly Negative.
Therefore, Natural Selection Eliminates the C Allele.
A Selective Equilibrium Will
Only Occur When p = 0 Under
Natural Selection For All Alleles.
A
pA = 1-pS
Genotypes
Viability Malaria
S
pS
AA AS SS
0.9
1
0.2
aA = (1-pS)(0.9-W)+pS(1-W) = 0 = aS = (1-pS)(1-W)+pS(0.2-W)
A Selective Equilibrium Will
Only Occur When p = 0 Under
Natural Selection For All Alleles.
A
pA = 1-pS
S
pS
aA = (1-pS)(0.9-W)+pS(1-W) = aS = (1-pS)(1-W)+pS(0.2-W)
(1-pS)(0.9)+pS(1) = (1-pS)(1)+pS(0.2)
0.9+0.1pS = 1-0.8pS
0.9pS = 0.1
pS = 0.1/0.9 = 0.11
So At Equilibrium, pS = 0.11 and pA=0.89
The Equilibrium Allele
Frequencies Are Maintained By
Natural Selection, Resulting in a
Balanced Polymorphism
A
pA = 0.89
S
pS=0.11
The Balance Occurs Because When pS < 0.11, aS > 0
(malarial resistance dominates the average excess)
And When pS > 0.11, aS < 0
(anemia dominates the average excess)
The Equilibrium
A
pA = 0.89
AA
0.79
WAA = 0.9
S
pS=0.11
AS
0.20
SS
0.01
WAS = 1
WSS
=0.2
At Equilibrium, There is Genotypic Variation in
Fitness (Broad-Sense Heritability), but No
Heritability (Average Excesses = 0).
Adaptation By Natural Selection
Depends Upon History:
Which Mutations Are Present and
Their Frequencies. The course of
adaptation is always constrained
by the available genetic variation
and proceeds until there is no
heritability of fitness.
Two Possible Responses to Malaria
A
pA 
p S  0 pC  0
A
pA = 0.89
S
pS=.11
C
pC = 1
1. The Fittest Genotype is Eliminated.
1. The Fittest Genotype is Fixed.
2. Average Fitness goes from .9 to .91.
2. Average Fitness goes from .9 to 1.3.
3. 20% of the individuals have a relative
viability of 1 and 80% have either
anemia or malarial susceptibility.
3. 100% of the individuals have a
relative viability of 1.3 and none have
anemia nor malarial susceptibility.
Two Possible Responses to Malaria
A
pA 
p S  0 pC  0
A
pA = 0.89
S
pS=.11
C
pC = 1
With One Exception
1. The Fittest Genotype is Eliminated.
1. The Fittest Genotype is Fixed.
2. Average Fitness goes from .9 to .91.
2. Average Fitness goes from .9 to 1.3.
3. 20% of the individuals have a relative
viability of 1 and 80% have either
anemia or malarial susceptibility.
3. 100% of the individuals have a
relative viability of 1.3 and none have
anemia nor malarial susceptibility.
Hb-A, S and C
Genotypes AA AS
SS
AC
CS
CC
Viability
No Malaria
0.2
1
0.7
1
1
1
S is a recessive,
deleterious allele
relative to A, so
natural selection in
the pre-Malarial
environment will
keep it rare (no h2).
C is a neutral allele
relative to A, so
sometimes the C allele
will drift to high
frequencies relative to
the A allele.
Suppose There Was A Deme With
This Gene Pool Before The
Malaysian Agricultural Complex
A
pA = 0.95
pS=.005
Such a gene pool is likely to evolve in the pre-malarial
environment because of the neutrality of A and C
relative to each other.
C
.045
Initial Phenotypes After Transition to
Malaysian Agricultural Complex
Genotypes
AA
AS
SS
AC
CS
CC
Viability Malaria
0.9
1
0.2
0.9
0.7
1.3
Genotypic Deviation
-.002 .098 -.702 -.002 -.202 .398
(W = 0.902)
aA = -0.001
aS = 0.081
aC = 0.015
The Initial Adaptive Response
To A Malarial Environment Is
To Increase The Frequency of
The S and C Alleles.
Gene Pool After Several
Generations of Selection Under A
Malarial Environment
A
pA = 0.78
.05
C
0.17
S
Genotypes
AA
AS
SS
AC
CS
CC
Viability Malaria
0.9
1
0.2
0.9
0.7
1.3
Genotypic Deviation
(W = 0.914)
-.01
.09
-.71 -.01 -.21 .39
Gene Pool After Several
Generations of Selection Under A
Malarial Environment
aA = -0.009
aS = -0.005
aC = 0.044
After the Initial Adaptive
Response To A Malarial
Environment, Natural
Selection Continues to
Decrease A, Increase C,
but Now It Also
Decreases S Because aS=
-0.005.
A Negative Correlation Exists Between the
Frequencies of the S and C alleles in Malarial
Regions in Africa
0.25
0.20
o.15
C
Allele
Frequency
0.10
o.o5
o.o
o.o
o.o5
0.10
S Allele Frequency in 72 West African Populations
o.15
Even uniform selective pressures
produce divergent adaptive
responses because selection
operates upon variation whose
creation and initial frequencies
are profoundly influenced by
random factors such as mutation
and drift.
Although adaptation is often
portrayed as “optimizing”
individual or population fitness,
only gametic fitness is optimized
via natural selection. Individuals
or demes with the highest fitness
are not necessarily favored and
can be actively selected against.
There are many other ways in which human populations
have adapted to malaria; e.g. G-6-PD Deficiency:
Plasmodium oxidizes RBC NADPH
from the Pentose Phosphate
pathway for its metabolism. This
results in a deficiency of RBC
GSH, most severe in G6PD
deficient individuals, leading to
peroxide-induced hemolysis which
curtails the development of
Plasmodium.
There are many other ways in which human
populations have adapted to malaria; e.g.
Thalassemia:
Adaptation generally involves
many loci with different
biochemical, cellular or
developmental functions.
Therefore, we also need to model
natural selection as a polygenic
process.
The Fundamental Theorem of
Natural Selection
• Fisher was one of the first to model
natural selection as a polygenic process.
• Although there are many aspects of his
models, the most important results are
found in what he termed the
“fundamental theorem of natural
selection.”
x = phenotypic value of some trait for an individual in a
population
f(x) = the probability distribution that describes the
frequencies of x in the population.
The mean phenotype is then:


xf(x)dx
x
w(x) = the fitness of those individuals sharing a common
phenotypic value x.
The mean or average fitness of the population is:

w

w(x)f(x)dx
x
w(x)f(x) does not in general define a probability distribution,
but w(x)f(x)/ w does integrate to one and defines the
probability distribution of the selected individuals.
Hence,
 the mean phenotype of the selected individuals is:
s 

x
xw(x)f(x)dx
w
Let h2 = the heritability of the trait.
The response to selection is given by R=h2S

where S=(s–), R = (o–), and o is the phenotypic mean
of the offspring of the selected parents.
When x = w, w(w) = w by definition, and  = w.

s 
s 

 w
w
2
w
w  wf(w)dw
w

 w 2 w 2 f(w)dw
w


  w
 w
w
2
w 2 f(w)dw
w
 w 2f(w)dw  w 2  f(w)dw
w
w
 ww  w f(w)dw  w 2  2  w 2
2
s 


S  s   
w
2  w2
w
w

w
2  w2  w2
w

2
w
w Hence,
When x = w, the response to selection, R, is .
R  h 2S

 a2  2 
w   2  
  w 
w 
 a2
w
Fundamental Theorem of Natural Selection

Some Implications of FFTNS
• FIRST, natural selection can only operate when
there is genetic variation associated with
phenotypic variation for fitness in the population.
• SECOND, the only fitness effects that influence the
response to natural selection are those
transmissible through a gamete.
• THIRD, the adaptive outcome represents an
interaction of fitness variation with population
structure.
Some Implications of FFTNS
• FOURTH, selective equilibria can only occur
when all the average excesses and all the average
effects are zero; that is, when all gamete’s have
the same average fitness impact. Evolution due to
natural selection stops only when there is no
heritability for fitness. This in turn means that at a
selective equilibrium there is no correlation
between the fitness of parents and the fitness of
their offspring even when there is genetic variance
in the phenotype of fitness.
The Equilibrium
A
pA = 0.89
AA
0.79
WAA = 0.9
S
pS=0.11
AS
0.20
SS
0.01
WAS = 1
WSS
=0.2
At Equilibrium, There is Genotypic Variation in
Fitness (Broad-Sense Heritability), but No
Heritability (Average Effects = 0).
Some Implications of FFTNS
• FIFTH, natural selection acts to increase the
average fitness of a population on a per
generational basis. Because the additive genetic
variation must be greater than or equal to zero, w
≥ 0 under natural selection. Because average
fitness can only increase or stay the same under
natural selection, the selective equilibria discussed
under point four must always correspond to an
average fitness local optimum.
Wright’s Concept of An Adaptive
Surface or Landscape
AA
AS
SS
WAA = 0.9
WAS = 1
WSS=0.2
AverageFitnes s
1.0
AverageFitnes s
0.92
0.8
0.91
0.6
0.90
0.4
0.89
0.2
p
0.0
0.2
0.4
0.6
Frequency of S
0.8
1.0
p
0.00
0.05
0.10
Frequency of S
0.15
0.20
Some Implications of FFTNS
• SIXTH, natural selection only takes
populations to local adaptive solutions and
not necessarily to the adaptive state with the
highest average fitness, and indeed may
operate to prevent an adaptive state with
higher average fitness from evolving.
Wright’s Concept of An Adaptive
Surface or Landscape
AA
Aa
aa
WAA = 1
WAa = 0.5
Waa=0.9
AverageFitnes s
1.0
0.9
0.8
0.7
p
0.0
0.2
0.4
0.6
Frequency of A
0.8
1.0
Genotypes
AA
AS
SS
AC
CS
CC
Viability Malaria
0.9
1
0.2
0.9
0.7
1.3
C
A
1.25
0.91
S
1
0.905
w
C
0.9
0.895
A
0.89
0.75
S
0.5
A
C
0.25
A
pA
pS
pC
C
pS
pA
pC
S
S
Some Implications of FFTNS
• SEVENTH, natural selection generally does
not optimize, even in a local sense, any
individual trait other than fitness itself, even
if the trait contributes to fitness in a positive
fashion.
w 0) at a local peak, let feq(x) =
Given a selective equilibrium (=
the phenotypic distribution of the trait at equilibrium. Then, the
average fitness and average trait at equilibrium is:

weq 
xeq 

x
w(x)feq (x)dx

xf
(x)dx
eq
x

xeq is the “optimal” value of trait X only if

weq  w(x eq )
 Use Taylor’s theorem to expand w(x) around x eq:
w(x)  w(xeq )  w'(x eq )(x  x eq )  1 2 w''(x eq )(x  x eq )2

Take the average value of both sides of the Taylor’s Series
approximation by integrating across the equilibrium probability
distribution of the trait:
weq  w(xeq )  x feq (x)dx  w(xeq )  x x  xeq feq (x)dx  12w(x
 eq )  x x  xeq  feq (x)dx
2
2
weq  w(xeq ) 12 w(x
)

 eq eq(x)

xeq is an optimal value of trait X that maximizes w(x) when:

1. the trait has no phenotypic variance at equilibrium
[2eq(x) = 0], or
2. the trait is related to fitness in a strictly linear
fashion at equilibrium [w”( xeq) = 0]
Some Implications of FFTNS
• EIGHTH, the process of adaptation can result in
the evolution of some seemingly non-adaptive
traits. In general, many traits contribute to fitness,
not just one. Consider the case in which two
traits, say X and Y, contribute to fitness such that
w(x,y) is the fitness of those individuals with trait
values x and y for the two traits respectively.
Then, the two-dimensional requirement for
optimality of both traits is:
 2w(x eq , y eq ) 2
 2w(x eq , y eq )
 2w(x eq , y eq ) 2
 eq (x)  2
Coveq (x, y) 
 eq (y)  0
2
2
x
xy
y
E.g., many human populations have adapted to malaria by
increasing the frequency of the trait of hemolytic anemia. Here,
natural selection favors the increase of a highly deleterious trait.
Such cases are common because of pleiotropy, and indeed most
of the people who die or suffer from genetic disease do so
because natural selection favored the genes despite one or more
pleiotropic deleterious traits.
Some Implications of FFTNS
• NINTH, the course of adaptive evolution is
strongly influenced by genetic architecture.
0.91
0.905
w
C
w
C
0.9
0.895
A
0.91
0.9
0.895
A
0.89
0.89
S
A
S
C
pS
pA
0.905
A
C
pS
pA
pC
pC
S
C recessive to A for malarial resistance
S
C with 4% dominance to A for malarial resistance
Common theme?
p = paA/W
w 

2
a
w
The Course of Adaptive Evolution Is
Determined By the Phenotypic Effects
Assigned to GAMETES, not individuals!
