Ecology 302: Lecture II. Evolution.
(Readings: Ricklefs, Ch.6,13. Gould & Lewontin, "Spandrels";
Johnston, Importance of Darwin)
“Synthetic” theory of evolution. Mutation is the source of heritable variation. Organismal phenotype is determined jointly by heredity and environment (what Darwin called the “conditions of life”). Differential reproduction and survival (“Darwin’s demon) alters the frequencies of
both phenotypes and the underlying gene frequencies.
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Key Points.
• Darwinism a theory of competition.
• Rediscovery of Mendelism facilitated fusion of the DarwinWallace selection theory and genetics.
• Modern Synthesis essentially a theory of gene frequencies
and factors that affect them.
• Consequences of diploidy.
• Hardy-Weinberg equilibrium and deviations therefrom.
• Absent mutation / migration, inbreeding increases with
consequent loss of genetic diversity.
• Selection changes gene frequencies so as to maximize .
• Quantitative genetics appropriate for metric characters under polygenic control.
• Heritability, 1 ⇒ “reversion to the mean”.
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• Effective population size reflects deviations of realworld population properties from those of an ideal population.
• Reaction norms map environment into phenotype.
• Adaptive “transgenerational effects” consequent to extrachromosomal (epigenetic) inheritance.
• Adaptive scenarios, while appealing, should be weighed
against non-adaptive alternatives.
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I.
Theory of Natural Selection.
A. Variability.
1. Some variations heritable.
2. Of these, some affect fitness.
B. Excess reproduction – Principle of Malthus.
C.
A + B => Descent with modification (DwM).
D. As articulated by Darwin / Wallace, a theory of competition.
Figure 1. Substitution of an advantageous mutant in a haploid. N1* and
N2* are equilibrium densities of wild type and mutant populations. a.
Per capita rates of increase (births – deaths) plotted against population
size. For all densities, the mutant outperforms the original. b. Numbers
of the two vs. time. Arrow marks origination of the mutant.
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E.
Rediscovery of particulate inheritance made possible
1. Reconciliation of the “selection theory” and inheritance – solved the loss of variability problem.
2. Elaboration of the “Modern Synthesis” after WWI.
F.
“Modern Synthesis” holds that
1.
Population genetics central; evolution is changing
gene frequencies.
2.
Mutation the source of heritable variation.
3.
Mutation rates affected by environment but random
with regard to fitness consequences.
4.
“Stuff” of evolution is mutations of small effect; mutations of large effect almost always deleterious.
5.
Natural selection the sole creative force.
6.
Sequential fixation of beneficial mutants solves the
“monkey typing Shakespeare” problem. See
http://www.blc.arizona.edu/courses/schaffer/182/g
eorge.htm .
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G. Synthesis rejects
1. Saltatory change, i.e., evolution by “hopeful
monsters”.
2. Direct environmental induction of heritable
adaptive traits (accepted by both Darwin and
Lamarck).
3. Inherent tendencies to
a. Increasing perfection / complexity (Lamarck’s “Power of Life”).
b. “Evolutionary momentum” (orthogenesis)
and its consequences (directional evolution; “racial senescence”) as observed, for
example, in the evolution of horses.
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II. Factors that Affect Gene Frequencies.
A. Selection.
1. Directional
2. Stabilizing
3. Disruptive.
4. See Ricklefs, pp.
119-23 for examples:
Darwin’s
finches; scale insects, etc.
Figure 2. Different modes of selection on a quantitative trait.
B. Mutation
1. Ultimate source of new variation.
2. Maintains deleterious alleles (that sometimes
later become advantageous) in the face of selection (mutation-selection balance).
C. Migration
1. Another source of variation.
2. The “glue” that holds populations together.
D. Population size. Stochastic loss of genetic diversity (“drift”) inversely related to population size.
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E. Diploidy introduces new possibilities.
1. Retards elimination of deleterious recessives,
2. Heterozygote advantage – maintains genetic
diversity – e.g., sickle cell gene in presence of
malaria.
3. Heterozygote inferiority – initial frequencies
determine the outcome.
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III. Mendelian Population Genetics.
A. Hardy–Weinberg (HW) Law.
1. Relates genotypic
frequencies
to
gene frequencies
2. Assumes
a. Infinite, panmictic populations.
b. No other forces operative.
3. Under these conditions, H-W frequencies established in a single
generation.
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Top. H-W frequencies result
from random mating between
male and female parents.
Bottom. Genotypic vs. gene
frequencies.
4. For one locus and two alleles: A, a, with frequencies p and q:
: : : 2: (1)
In finite populations, one encounters an excess of homozygotes that (again absent other
forces) increases from one generation to the
next.
; 2 2
(2)
1. Inbreeding coefficient, F, a measure of homozygote excess.
2. Often estimated from heterozygote deficiency
!"#$ !"%&'
!"#$
(3)
3. Absent new genetic variation, excess homozygosity, and hence F, increases with time.
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4. Define index of panmixia
() 1 )
(4)
5. It can be shown that
1 )
() *1 + ⇒ lim () 0; lim ) 1
)→/
)→/
2
(5)
6. Expected time to homozygosity (coalescence
time) is 4N generations.
7. Loss of variation ⇒ inbreeding depression.
8. With recurrent mutation, ) → 1 where
1
1 43 1
and μ is the mutation rate.
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(6)
B. Response to Selection.
1. In the case of one allele and two loci, change
in gene frequency, ∆, given by
7
51 6 8
∆ 7
8
2
(7)
where p is the frequency of one allele, and
7 9 251 69 51 6 9
(8)
is mean fitness of the population.
2. Eq 7 assumes H-W frequencies (weak selection).
3. Eq 7 => three possible equilibria:
0; 1; 0 ∗ 1
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(9)
a. Third possibility requires that
7
;$
=
;< <><∗
0
(10)
b. Eq 7 => gene frequencies change so as to
increase .
Fitness Relations
Response
9 ? 9 ? 9
) → 1
9 9 9
) → 0
9 9 ? 9
) → ∗ , 0 ∗ 1
9 ? 9 9
) → 0 or B) → 1
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Figure 3. Under selection, gene frequencies (left) change so as
DDD (right). Shown here are the four cases in Table
to maximize C
1.
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C.
Adaptive Topographies.
1. With multiple fitness
peaks, a population
can be stranded on
one
peak
even
though “jumping” to
another would increase fitness.
2.
Figure 4. 1-D fitness landscape.
Selection can keep the popula“Peak hopping” faciltion in the vicinity of one of the
itated by
two adaptive peaks.
a. Increased within-population variability;
b. Small population size, which facilitates stochastic
variation in gene frequencies (drift).
c. Environmental shifts whereby a population near
one adaptive peak finds itself on the slope of a different peak.
3. Key Point: Tension between deterministic and random forces.
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Figure 5. Evolution on a 2-D adaptive landscape. Dotted lines are contours
of equal fitness. Plus signs indicate fitness maxima; minus signs, minima.
Left. Increased mutation or reduced selection leads to increased genetic
variability. Center. Increased selection or reduced mutation reduces variability. Right. An environmental shift can place a population on a new peak,
which selection then causes the population to climb. Reduced population
size has the same effect as increasing mutation / reducing selection. From
Simpson. 1944. Tempo and Mode in Evolution.
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IV.
Quantitative Inheritance.
A. Most so-called “metric traits” controlled by multiple alleles.
1.
Length, weight, etc.
2.
Agricultural yields.
B.
The stuff of micro-, but probably not macro-evolution.
C.
Character distribution often approximately normal.
E 1
F√2H
!
I
5JIK6L
M L (11)
D. Quantitative genetics partitions phenotypic variance
into genetic and environmental component, and further subdivides genetic variance.
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E.
Heritability, h2, of a
trait, is the slope of the
regression, offspring
trait value vs. parent
value.
1.
Expected offspring
trait value given
by
Figure 6. Offspring vs. parental
height as determined by Sir Francis Galton in 1889.
N%OO ND PND<Q NDR
(12)
2.
1 ⇒ “reversion to the mean”.
3.
High heritability does not necessitate that variation in the character in question is largely under
genetic control.
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F.
Following truncation selection,
established but shifted.
distribution
Figure 7. Re-establishment of trait distribution
after truncation selection.
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re-
G. Historical note: Demonstration1 by R. A. Fisher that
“continuous” variation of metric traits consistent with
polygenic control
1.
Made possible the reconciliation (Modern Synthesis) of Mendelian genetics and Darwin-Wallace
theory.
2.
Rescued Darwinism from history’s ash heap.
Table 2. Mendelian vs. Quantitative Genetics.
Within
Genotype
Between Genotype
Variability
Variability
Mendelian
Small
Large
Quantitative
Large
Small
Appropriate
Genetic Model
1. 1918. The correlation between relatives on the supposition of Mendelian inheritance. Phil. Trans. Roy. Soc. Edinburgh.
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V. Finite Population Effects.
A. Hardy-Weinberg
frequencies only obtain in
the limit of infinite population size.
B.
In a finite population,
one observes an excess
of homozygotes.
C.
Genetic drift ⇒ loss of
genetic diversity and the
fixation of maladaptive
Figure 8. Simulation of genetic
alleles.
1.
drift of 20 unlinked alleles in
populations of 10 (top) and 100
Results from the (bottom). Loss of alleles is more
probabilistic na- rapid in the smaller population.
ture of births and
deaths.
2.
Most important in small populations in presence
of weak selection.
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D. Selection vs. Drift.
1. Probability of a
mildly beneficial
mutation’s being
fixed is ~2s, where
s is the selective
advantage.
2.
Probability of al- Figure 9. For N = 500,-3selection
dominates drift if s » 10 .
lelic fixation by
chance is 1/2N.
3.
Then selection more important than drift if
1
S≫
2
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(13)
VI.
Effective Population Size, UV .
A. Ideal population characterized by
1.
Random mating
2.
Equal numbers of males and females
3.
Constant population size.
B. , the size of an ideal population with same properties of the real one.
C. Factors that reduce .
1.
Assortative mating (likes mate with likes) – homozygotes accumulate in excess of HW proportions.
2.
Unequal sex ratio.
3.
Fluctuating populations – Special cases: bottlenecks, founder effect.
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VII. Phenotypic and Developmental Plasticity.
A. Behavioral. Individual responses to environmental stress promote homeostasis.
1. Diurnal variations in behavior.
2. Seasonal variation in diurnal rhythms.
3. Commonly observed in, but not restricted
to, poikilotherms.
B. Development. Reaction norms (RNs).
1.
RNs map environment
into
phenotype (Fig.
10).
2.
RNs often dffer
bewtween
genotypes
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Figure 10. Linear reaction norm
(hypothetical).
3. Between-population differences in RNs can
be adaptive responses to differences in average prevailing conditions.
Figure 12. Schematic illustrating adaptive variation in reaction
norms of two populations raised under different conditions.
Individuals have greater fitness in the environment in which
they were raised and reduced fitness in the other environment,
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VIII. Direct Environmental Induction.
A. Maternal exposure to
environmental triggers
can induce adaptive
changes in offspring.
B.
Trigger often a chemical
released by predators.
C.
Examples.
1. Immobile crickets –
avoid wolf spiders. Figure 13. Colored scanning elec2.
tron micrograph of different
Helmeted
water forms of the water flea Daphnia
fleas – frustrate cucullata. Left. Standard shape.
predatory Chaobo- Right. Predator-induced morph
with helmet (green) and tail
rus larvae.
(blue). From Sciencephoto.com.
D. In some cases, effects
transgenerational
E.
Mechanism appears to be epigenetic, e.g., changes in
DNA methylation, that affect gene expression.
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XI. Evolution and The Adaptationist’s Programme.
A. Theory of evolution
really two theories.
1.
Descent
with
modification
(DwM) – the macroscopic pattern.
2.
(Heritable) Variation plus selection
(VpS) – the presumptive
proximate mechanism.
Figure 16. Phylogenetic descent as envisaged by Lamarck in his Philosophie Zoologolique (1809). Infusoria (protists), (hydras) polyps and radiaria (jellyfish) form one
group. All other animals descend from worms.
B.
With regard to DwM,
evidence has continued to accumulate
since the days of Lamarck.
C.
With regard to mechanism, ideas have continued (and are continuing) to change.
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D. George no longer limited to typing one letter at a time.
E.
Desire to shoehorn observations into adaptive scenarios understandable. But …
1.
2.
The evidence is often weak.
Figure 17. Spandrel in St. Mark’s
non- cathedral in Venice.
There are
adaptive alternatives – see Gould and Lewontin.
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