Download Phenotype/Genotype Phenotype/Genotype cont. The sickle cell

We have been discussing genetics (as they
inform our understanding of evolution (and
later, conservation biology and the applications
of biotechnology in agriculture)
DNA/RNA
Nucleotides
Chromosomes
Genes
Mutations
Alleles
Genotypes/phenotypes
Gene expression
Dominant/recessive
We can use human blood groups to illustrate a
number of genetic factoids
Human blood groupings: another aspect of alleles
1.
Human blood types are also an example of
different alleles in a population
Everybody has a gene for blood type (meaning
everybody has two alleles for blood type), but
we don
don’tt all have the same two alleles.
alleles
There are four major blood proteins among
humans: A, B, AB and O each of which is coded
for by different sequences of nucleotides which
lead to different sequences of amino acids.
2.
3.
4.
5.
6.
1
2
Phenotype/Genotype
The human gene pool contains three blood
alleles: A, B and O
A is dominant over O, B is also dominant over O (but A
and B are “co-dominant”).
This means that the A or B allele will always be
“expressed” and can mask the effects of the O allele.
S an iindividual
So
di id l with
ith EITHER 2 A alleles
ll l or 1 A and
d1O
will “express” (have) type A blood.
An individual with EITHER 2 B alleles or 1 B and 1 O will
have type B blood.
An individual with one A and one B allele will have AB
type blood
Since O is masked by A and B, individuals with type O
blood have to have two O alleles.
4
Humans, gorillas, orangs, horses, dogs,
and pigs all have characteristics similar
to the A, B and O alleles in their
populations:
So, blood “types” (and multiple alleles)
appear to be characteristic of all mammals
• AA and BB are referred to as homozygous dominants
• OO is referred to as homozygous recessive (the equivalent of the
“spirit bear”)
2 different alleles are referred to the heterozygous
genotype
• AB, AO or BO
There is no strong evidence of a selective
advantage or disadvantage to any particular
blood type
Is this true of all alleles
NO!
7
Homozygous dominants (AA or BB) share the same
phenotype as the heterozygote (AO, BO)
While they “look” alike, they represent different
genotypes
One measure of the genetic diversity of a
population is allele frequency (how many alleles are
present in the entire species gene pool),
recognizing that each individual in the pool can
only have 2 of the possible suite of alleles.
(NOTE: sometimes there is only one allele in a
population and every individual in a population is
homozygous with respect to that characteristic – an
extremely conservative characteristic)
5
While there are a number of known HBB gene
variants, sickle cell anemia is most commonly caused
by the hemoglobin allele Hb S. In this allele, the
amino acid valine takes the place of glutamic acid
• suggesting that this characteristic appeared long
ago in mammalian evolution
3
Phenotype/Genotype cont.
The type of blood you have (what is expressed) is called
your phenotype – what you “look” like (phaino Gk for
show)
The alleles controlling that expression are your genotype
So there are 4 blood phenotypes: Type A, Type B, Type
AB and Type O
B there
But
h
are 6 genotypes: AA,
AA AO,
AO BB,
BB BO,
BO AB and
d OO
2 identical alleles are referred to as the homozygous
genotype (AA, BB, OO)
Locus: The HBB gene is found in region
15.5 on chromosome 11.
Gene Structure: The normal and sickle
allelic variants are 1600 base pairs (bp) long
Protein Size: The HBB protein is 146
amino acids
Does it “matter” what blood group you are?
In sexually reproducing organisms (humans and many other
species), chromosomes come in pairs.
This means that a particular genetic characteristic is also paired
(one version or allele on each chromosome)
These two alleles could be the same but there could also be a
different allele for the same characteristic on each
chromosome.
Some alleles (referred to as dominant) are always “expressed”
and they “mask” the effects of other alleles (referred to as
recessive)
There are actually only three different blood group alleles in the
human gene pool (all the genes in all humans taken together),
but each of us can only have 2 of those 3 alleles.
Which pair of alleles we end up with (and whether we have 2
dominant alleles, one dominant and one recessive or two
recessive alleles) determines what “type” blood each of us has.
8
6
The sickle cell allele is dominant
Let’s call the allele for regular hemoglobin s
Let’s call the allele for sickled hemoglobin S
S is dominant, s is recessive.
People with two ss alleles will have normal
hemoglobin
hemoglobin.
People with SS alleles will have crenulated red
blood cells and be very ill. Before the advent of a
successful medical management regime, most
people died (often in utero or shortly after birth)
People who are heterozygous, Ss, will have some
% of crenulated cells and may experience periodic
crises but will usually survive – particularly today
with advantaged medical intervention
9
1
If sickle cell anemia is (or at least was) a lethal
mutation, why didn’t it ‘disappear’?
Logically, you would think that a mutation
creating an allele that changes the shape of the
red blood cell and has life-threatening
consequences (the sickled form of the cell hangs
p in capillaries)
p
) would not “persist”
p
(i.e. p
people
p
up
with this condition would die young, not
reproduce and eventually the allele would
disappear).
But this isn’t how it worked!
Why is the allele still around and of major
concern to people of African ethnic origin?
10
Speciation and extinction govern biodiversity
Sickle Cell Anemia: practicing vocabulary
The sickle cell allele is dominant
• Individuals who are homozygous for normal haemoglobin
(and normal red blood cells) are homozygous recessive - ss
• Individuals who are homozygous dominant for the sickled
haemoglogin and sickled red blood cells are SS – they
express sickle cell anemia and before the advent of medical
intervention they would have died.
intervention,
died
• However, before the advent of anti-malarial drugs,
individuals who were heterozygous (Ss) suffered from partial
sickle cell anemia, were not well, but it turns out they were
less susceptible to malarial parasites (!)
Consequently, ss individuals died from malaria, SS individuals died
from sickle cell anemia. However, Ss individuals suffered but
many survived to reproduce so the S allele persisted and was
actually selected for! (Heterozygote advantage)
11
Fig 3.6 (KR#8)
1. The vast majority of species that have lived on
Earth are gone
2. The fossil record suggests that species persistence
averages 1 – 10 million years
3 Extinction is a natural process (see Fig 3.6
3.
3 6 & 3.7
3 7 in
KR#8) but humans are affecting its rate.
4. Evidence supports 5 past mass extinction events
(losses of 50 - 95% of Earth’s extant biodiversity)
5. Many biologists believe that we are entering the
6th mass extinction event and it is being caused by
humans – the concern is persistence of ecosystem
services that we and all species require
13
Peter and Rosemary Grant have studied Darwin's
finches since 1973
When rainfall, and thus food, are
plentiful, the finches:
These futuristic looking
organisms lived over 530 million
years ago
You can see their fossilized
remains at Yoho National Park
in BC
The Burgess Shale fossils - the
world’ss most famous ancient
world
marine ecosystem – played an
important role in understanding
the complexity of evolving life
systems
Yet they are unrelated to any
later living forms and their
disappearance presents an
intriguing mystery
14
However, in 1976-1977, a severe
drought struck the Galapagos
16
Mutations (whether from “mistakes” or induced by mutagens)
can lead to different “versions” of the same gene (alleles)
While the absence of a critical protein could be deleterious, it
is also possible that a new protein created by a mutation could
be advantageous or have no effect what-so-ever
The peppered moth, human blood types and sickle cell anemia
were examples of different alleles in a population with
different outcomes
• the presence of different wing colour alleles turned out to be
advantageous for the peppered moth when the environment changed
• the mutations that lead to different alleles for human blood types (a
polymorphism*) seems to be neutral
• there are also different hemoglobin alleles in the human gene pool however the mutation that lead to this is deleterious: sickle-cell anemia
- however, heterozygotic advantage maintains this deleterious allele in
the gene pool.
12
The Case Study of Darwin’s Finches
13 species of finches found only in the Galapagos Islands and
nowhere else on earth – DNA suggests these diverged from a single
ancestral group of birds that arrived on the islands
Some finches have stout beaks
for eating seeds of one size or
another (#2, #3, #6).
Others have beaks adapted for
eating insects or nectar.
One (#7) has a beak like a
woodpecker's. It uses it to drill
holes in wood, but lacking the
long tongue of a true
woodpecker, it uses a cactus
spine held in its beak to dig the
insect out.
One (#12) looks more like a
warbler than a finch, but its
eggs, nest, courtship behavior,
and (most importantly) its DNA
tell us it is closely related to the
other finches.
15
One of the few plants to make it through the
drought produces seeds with large, tough shells
that are virtually impossible to open for birds with
beaks smaller than 10.5 mm
Sampling the birds that starved as well as those
that survived showed that the birds that survived
were those with larger beaks
The drought
caused a precipitous
decline in the
production of the seeds
that are the dietary
mainstay of a particular
f h (the
finch
( h medium
d
ground finch)
The graph shows how
the population of this
finch species declined
from 1400 to 200 on
one island in the
Galapagos
• have a varied diet, e.g. eat seeds across a
range of sizes and
• show considerable variation in body and
beak sizes (large beaks are better for large
seeds but can handle small seeds as well
as birds with smaller beaks).
Mutation is a source of genetic
diversity!
17
18
2
natural selection (and microevolution) at
work
As the population recovered after
the rains returned, the average
beak depth of the population was
greater than before (an increase of
4–5%)
4
5%)
Birds with bill sizes greater than
the mean survived
Birds with bill sizes less than the
mean died
The curve showing the distribution
of beak sizes had shifted
Other sources of genetic diversity
1. Cross-over: occurs during cell reproduction
Two cell division processes
Mitosis (cell cloning)
1. Cross-over (and recombination)
2. Sexual reproduction
• Cell division that produces two identical
daughter cells (the kind of cell division
growth & cell replacement)
p
)
associated with g
a. Independent assortment
b. Random fertilization
3. Transposable genetic elements
(transposons), “jumping genes” or
“genetic instability”
beak size
•
Meiosis (gamete or egg and sperm
production)
• Cell division that produces daughter cells with
half the original number of chromosomes (the
kind of cell division associated with
reproduction or production of new individuals)
a naturally occurring phenomenon that is
nevertheless remarkably similar to
genetic engineering technologies
19
20
When cells reproduce they have to replicate
everything inside themselves including their
chromosomes
Meiosis: start out with one
cell (with 4 chromosomes).
End up with 4 cells that
each have half the number of
chromosomes of the original
parent, i.e. 2 chromosomes
This example also shows
“cross-over,” a phenomenon
that sometimes accompanies
chromosome duplication
(whether in meiosis or
mitosis) and produces
genetic diversity!
Mitosis: start with a
single cell (with 4
chromosomes) and end
up with 2 cells that are
identical copies (4
chromosomes each)
Most cells are doing mitosis - “cloning” themselves – making more of exactly
the same kind of cell in the normal process of growth or cell replacement.
However sexual reproduction requires a special kind of cell reproduction
(meiosis) that produces specialized egg and sperm cells.
22
Of the 4 gametes
produced by
meiosis in this
example, 2 have
a genetic
sequence
identical to the
parent cell (ace
and bdf) no bits
swapped places!!
But 2 of the
gametes contain
unique genetic
sequences, unlike
those of the
parent cell (acf
and bde)
25
Note that the word
mitosis has a “t” in
it for “2” ☺
23
How closely a child resembles a parent depends
upon which of these gametes are fertilized
Original chromosome
(genetic sequences) of a
parent
21
A child created from an egg or
sperm containing this chromosome
will be more like one parent than a
child from an egg or sperm
containing this chromosome who
has a unique genetic sequence
26
Notice how tiny
red and blue bits
swapped places?
Note that the word
meiosis has a “o”
in it for “1” ☺
24
Cross-over can create genetic diversity
These mules are identical twins (they are the result of a single
fertilized egg that divided prior to beginning embryonic growth).
Mitotic cross-overs as they grew generated slightly different
pigment patterns – even identical twins don’t have perfectly
identical DNA, butThese
we might
never
be able totwins
find those small
mules
are “identical”
27
differences among the billions of base pairs
3
What’s the point of cutting chromosome
number in half?
2. Sexual reproduction: independent
assortment and random fertilization can
also create genetic diversity
Is there any pattern to how chromosome number
is cut in half?
Humans have 23 pairs of chromosomes in
each cell of our bodies (except our egg and
sperm cells)
IF there were no process to cut the number
of chromosomes in half, fertilization of eggs
b sperm would
by
ld lead
l d to
t a doubling
d bli off
chromosome number!
So meiosis creates eggs and sperm cells with
only 23 chromosomes (rather than 23 pairs)
Fertilization restores the correct number of
chromosomes to 46 (23 pairs)
Recall meiosis – the
type of cell division
that cuts chromosome
number in half.
28
Human “karyotype”
1A and 1B, 2A and 2B, 3A
and 3B etc.
How many different
“versions” of a gamete could
we make with 23 pairs of
chromosomes if each pair
splits independently?
Transposons (jumping genes)
34
Will all the
starred versions
end up in the
same egg or
sperm?
*
*
*
*
*
*
29
A gamete (egg or sperm) is not a new individual!
We need two gametes (to restore the correct
chromosome number)
Each of those 8 million + gametes has an
equal chance of being fertilized by one of
8 million + other gametes
8,388, 608 x 8,388, 608 =
70, 368, 744, 177, 644
Each of us is a 1 in 70 trillion event (!)
31
Similarly to cross-over, transposons can create new alleles by inserting
themselves into established coding gene sequences (changing the
nucleotide sequence at the locus they have just left as well as the
sequence where they now reside)
They can also act epigenetically - affecting the expression of genes at
other loci
Transposons are similar to retroviruses a fact which has lead some
people to speculate that transposons came from viruses that
p p
host DNA and are still there!
expropriated
We know that antibiotic resistance is conferred by transposons that start
jumping around in the presence of antibiotics (in other words antibiotics
repress the “repressors”)
Transposons can also jump between species (among “species” or strains
of viruses or bacteria, between viruses/bacteria or to other species
including humans)
As we discussed in our environmental health lectures, E. coli 0157H7
appears to have acquired its virulence from a gene that “jumped” from
the bacteria that causes cholera to the originally benign E. coli probably
via a retrovirus
NO! Each pair
splits
independently
30
3. Transposons or jumping genes can also
create genetic diversity
Gene fragments (~750 to 2500 base pairs)
found in the so-called “junk” DNA have no
fixed location (locus) – they can move around
spontaneously, although they appear to be
under the control of “repressors” that keep
them reasonably quiescent
These are not p
part of either the genome
g
or
epigenome, so they are still referred to as
“junk” but that means we just don’t yet
understand the function of this type of DNA
which is neither coding nor non-coding DNA
Barbara McClintock, 1902Jumping genes/transposons often appear to
1992, discovered jumping
be repeated nucleotide segments (e.g. a
genes in maize in 1948. She
sequence of base pairs, repeated over and
was awarded a Nobel Prize for
over and over again)
the discovery (1983)
Ubiquitous (found in the genome/epigenome
of every species investigated)
32
Given individual genetic diversity, what
mechanisms (besides natural selection) can
change allele frequencies in a population, i.e.
can lead to evolution (whether micro or macro)
So … genetic diversity can derive
from
1. Mutation (spontaneous or induced)
2. Cross-over during cell reproduction
3 Sexual reproduction
3.
•
•
2 other “evolutionary” mechanisms
generally accepted as forces
alternative to natural selection:
Independent assortment
Random fertilization
1. non-random matings (sexual selection)
2. genetic drift
can also change allele frequencies – in a
population
4. Transposable genetic elements
(jumping genes)
NOTE: changes in genetic diversity are happening at the
level of an individual’s genetic material!
33
35
36
4
The diversity that derives from independent
assortment and random fertilization (2)23 in
humans assumes random matings among
individuals
Individuals may choose mates in a non-random
manner
Under sexual selection (or active mate choice)
individuals choose mates as a result of
Do humans exhibit sexual selection?
Why choose a mate and who chooses?
Males produce millions of sperm. “Fitness”
suggests they should either:
Absolutely! The data are particularly clear for both
visual and olfactory (pheromone ) ‘signaling’
• attempt to copulate with as many fertile females
as possible or
• form a pair bond if they are assured of mate
fidelity
• Rikowski and Grammer* compared ratings of body
odour, attractiveness, and measurements of facial and
bodily asymmetry of male and female subjects.
• Subjects wore a T-shirt for three consecutive nights
under controlled conditions.
Females' eggs are few, thus females’ “fitness”
suggests they should be selective:
• theyy have more invested in each g
gamete and in
each resulting offspring
• they should seek out males who will invest
resources in their offspring
• male/male competition (aggression)
• male display and female mate choice
• female/female competition
• Shirts worn by males were given to females and vice versa for
the ‘snift’ test, i.e. what’s your reaction to this smell?
• Rated photos of the subjects for “attractiveness.”
• Additionally, bodily and facial symmetry of the odor-donors
were measured.
Since the availability of eggs is what limits
reproductive success (fitness), evolutionary
biology tells us that it’s generally males who
compete for female attention and females who
choose not vice versa
Sexual selection in humans is complicated by
cultural influences on “desirability”
pheromones: chemical messengers sent outside the body that evoke
physiological or behavioral changes in another member of the species
Therefore males often have exaggerated secondary sexual
traits to increase attractiveness to the opposite sex
37
The results?
38
Fitness and Genetic Load
For women, facial symmetry, ‘attractiveness’ and perceived
‘sexiness’ of body odour were significantly + correlated.
For men, ‘attractiveness’ and symmetry were + correlated
but body odour was only important if females were in the
most fertile (i.e. ovulatory) phase of their menstrual cycle.
However there were distinct preference patterns:
• Human pheromones are under genetic control with the particular
pheromones secreted by any individual a function of the genes that
code for our immune system or major histocompatibility complex
(MHC – recall our lectures on environment and health!).
• Humans can detect self odours (genetically similar MHC) versus
non-self odours (genetically dis-similar MHC) finding non-self odours
more appealing, i.e. opting for genetic diversity in a mate.
Why mate with someone genetically dissimilar?
40
Each of us carries 5 to 8 lethal alleles which, if homozygous, would
likely cause death. (The presence of lethal, sublethal and subvital
genes in any species is expected since mutations, cross-over and
random fertilizations mean not all individuals will be maximally fit.)
The more lethal alleles found in a population, the greater its genetic
load (The difference between the fittest genotype of a population and
g fitness of that population)
p p
)
the average
Inbreeding among individuals carrying a genetic load will increase the
frequency of 2 individuals with similar deleterious alleles mating –
increasing homozygosity of deleterious alleles
As homozygosity rises through inbreeding, a positive feedback loop
known as inbreeding depression sets in - characterized by reduced
survival of offspring, low birth weights, and infertility among other
things. (Anybody who breeds dogs, cats or fancy goldfish already
knows this!)
Random (stochastic) changes in allele frequency
result from the fact that only a tiny fraction of all
possible zygotes are going to become adults
Remember that you (and your siblings) are random
selections out of yyour p
parents potential
p
pool
p
of 70,,
368, 744, 177, 644 possibilities
In large populations, which particular gametes
actually fertilize each other does not have much
impact because the random nature of the process
tends to average things out over successive
generations
But what if populations are small?
43
e.g. hemophilia in
european royal
families
41
In small populations, gene frequencies can
change randomly in a process known as
genetic drift
Reach into a pile of pennies and pull out six. If
there were five heads and one tail or 4 heads
and 2 tails, you would not be particularly
surprised
p
However if you pulled out 600 pennies, we
would expect the results to be closer to 300
heads, 300 tails (e.g. we really don’t expect
400 heads and only 200 tails)
In a small sample, chance can cause a
departure from the expected result
2. Genetic drift: changes in allele frequency
resulting from chance
* Proc R. Soc. Lond. Biol Sci. 1999; 266:869-74
44
39
Queen Victoria arranges
marriages for her children and
grandchildren with royal families
of Europe (to strengthen
political ties).
In Spain and Russia, the plan
backfires leading to political
unrest as the royal children are
discovered to be hemophiliacs anti-British sentiments are
fueled as the blood of Britain is
considered “tainted.” (In Russia,
Rasputin is believed to have
come to power primarily
because Czarina Alexandra was
so unhinged over her
hemophiliac son, Alexis.)
Interestingly, this particular
mutation seems to have started
with Victoria as hemophilia was
unknown in her ancestors.
42
In the next generation . . .
This process of random fluctuation continues generation
after generation, because the population has no "genetic
memory" of its state
Each generation is an independent event.
However as an allele’s frequency decreases, it could
become less likely to be sampled and a positive feedback
process sets in where the allele continues to spiral down
in ffrequency
eq enc (assume
(ass me a pop
population
lation of 100)
100).
•
•
•
•
•
50 heads/50 tails (pull out 10: 6 heads/4 tails)
Next generation: 60 heads/40 tails (pull out 10:
Next generation: 60 heads/40 tails (pull out 10:
Next generation: 70 heads/30 tails (pull out 10:
Next generation: 80 heads/20 tails (pull out 10:
6
7
8
9
h/4
h/3
h/2
h/1
t)
t)
t)
t)
It is possible that an allele could disappear completely
simply as the result of random chance.
45
5
Why might we care if drift changes allele
frequencies in small populations (particularly why
should we worry about the risk of allele loss)?
It’s genetic diversity that allows organisms to adapt to
change
If environmental conditions change, the population may not
have any significant ability to “respond” (evolutionarily) to
the changed
g conditions (if
( theyy have no underlying
y g diversityy
for natural selection to work on).
Concern wrt genetic drift helps us understand the definition
of a minimally viable population (MVP) - 50 breeding pairs
and 500 individuals - is the minimum population size that is
statistically “immune” to genetic drift for about 100 years
(depending on generation time).
To protect extant genetic diversity in perpetuity, populations
need to have between 2500 and 5000 individuals.
Small populations (subject to drift) can arise from
founder effect – particularly of concern when we
try to re-constitute a population from just a few
individuals (or when only a few individuals
survive some severe impact)
Imagine that you and 9 other people are the only
survivors of the human race (or the 10 of you end up
traveling to Mars).
Your group cannot possibly contain the full genetic
diversity of all humans on the planet
Nevertheless (assuming the group has both sexes), you
could form a breeding population.
After many generations there might be millions of
people.
But this second human race would be substantially
genetically different from our current human race
reflecting the genetics of the “founding” individuals.
46
• The team concluded that 75% of
human genetic variation is the result of
random genetic drift in small founder
populations that left ancestral
homelands.
• Only ~25% of human genetic variation
stems from other sources
47
48
Lions of Ngorongoro Crater,
Tanzania
• In 1962 a plague of biting flies
killed almost all the lions in the
park (leaving 9 females and 1
male)
Thi population
l ti is
i geographically
hi ll
• This
restricted to the Crater which cuts
off emigration/immigration
• While the population has rebuilt
to approximately 125 individuals,
their allelic diversity is different
and much lower than that of lion
populations in other locations
50
Numerous sources of
genetic diversity
TORREY pine (Pinus torreyana)
Mutation
Cross-over (and
recombination)
Sexual reproduction
The rarest pine in the world with
<10,000 individuals existing in
only two populations in southern
California
P. torreyana may have been
reduced to <50 individuals 8500–
8500
3500 years BP – likely as a result
of post-glacial climate change
It exhibits the lowest genetic
diversity of any tree species
known
52
http://news.nationalgeographic.com/news/2005/10/1018_051018_human_origins.html
Examples of species that have passed
through genetic bottlenecks
49
By the 1890s only about
20 survived.
Elephant seals breed in
harems, with a single
male mating with a group
of females,, so one male
may have fathered all the
offspring at the extreme
bottleneck point.
The population today has
expanded to about
The concern – from a biodiversity
30,000, but biochemical
perspective - is the ability of this
analysis shows that all
population to respond to
elephant seals are
environmental change!
virtually genetically
identical.
www.eco-pros.com/biodiversity-genetic.htm
Ramachandran and her colleagues
studied the genes of 53 indigenous
populations around the world.
Y chromosome diversity of humans
The elephant seal was hunted almost to
extinction in the 1800s
Sohini Ramachandran, a doctoral
candidate in evolutionary biology at
Stanford University, was lead author of
a study published in the November
2005 Proceedings of the National
Academy of Sciences.
founder effect can be important when a small
group of individuals leaves to “found” a new
population in a new environment but it can also
be important when a catastrophic event reduces
a population to a few survivors (a sub-set of
original genetic diversity): the event is termed a
genetic bottleneck
g
From a laboratory exercise
designed by Bill Armstrong
Founder effect/genetic drift is assumed to be
the explanation for human genetic differences
The concern – from a biodiversity
perspective - is the ability of this population
to respond to environmental change!
• Independent assortment
• Random fertilization
How can we use this
information to help conserve
species (biodiversity) or the
implications of (agricultural)
biotechnology?
Transposable genetic elements
(transposons), “jumping
genes” or “genetic instability”
Number of mechanisms
capable of changing allele
frequency (evolution)
Natural selection
Non-random mate choice
Genetic drift
53
The concern – from a
biodiversity perspective is the ability of this
population to respond to
environmental change! 51
But before we can do that
we need to understand
how those organisms
present at any particular
time interact: “the
ecological stage, the
evolutionary play” in the
words of G.E. Hutchinson
Karen will start here next week!
54
6