Examples of Natural Selection in
action
Peppered Moth
Darwin’s Finches on Daphne major
Sickle Cell Anemia and Malaria
HIV and drug resistance
Peppered Moth and industrial
melanism.
Peppered moth occurs in two forms: light,
speckled form and dark (melanic) form.
In early 1800’s in Britain dark form very rare.
Dark form caused by a dominant mutation
that occurs spontaneously.
Dominant Mutation
A mutation is a change in gene’s DNA .
A dominant allele is expressed even if only
one copy is present. (i.e., is expressed
even in heterozygotes).
Peppered moths rest on trees and depend
on camouflage for protection.
Peppered Moth
In unpolluted areas trees covered in lichens. Light
form of moth hard for birds to see.
In mid 1800’s air pollution in British cities
covered trees in soot on which the dark form was
harder to spot.
In cities dark form of moth became common and
light form rare.
Peppered Moth
In mid 1950’s pollution controls reduced air
pollution in Britain and lichens began to
grow on trees again.
Frequency of dark form of peppered moth
has declined steadily since then.
Darwin’s Finches on Galapagos
Islands
Peter and Rosemary Grant of Princeton
have studied Medium Ground Finches
on Daphne Major for almost 30 years.
Banded and measured the island’s
entire population and followed it over
many years.
Darwin’s finches
Rainfall on Galapagos Islands is unpredictable.
In wet years, lots of seeds produced by plants but
in dry years few or no seeds produced.
When there is no rainfall the fixed supply of seeds
on the island must last the birds on the island until
the rains come again.
Beak size and feeding efficiency
Finches with larger bills can crack and eat
large seeds and small seeds.
Finches with smaller bills cannot eat open
very large seeds, but are more efficient at
eating small seeds.
In droughts large-billed finches (and genes for large bills)
survive better than small-billed finches (and genes for
small bills) because when all the small seeds have been
eaten they can still open the remaining large seeds.
When there are lots of seeds available, small beaked birds
do better than large beaked because they can collect and
process small seeds faster.
Mean beak depth of the finch population fluctuates in
synchrony with rainfall patterns.
Sickle Cell Anemia
Sickle cell anemia is a condition common
in West Africans (and African Americans of
West African ancestry).
In sickle cell anemia red blood cells are
sickle shaped under low oxygen conditions.
If left untreated the disease is usually fatal by
about age 10.
Sickle cell anemia
About 1% of West Africans have sickle cell
anemia.
A single mutation causes a valine amino acid to
replace a glutamine in an alpha chain of the
hemoglobin molecule.
Mutation causes molecules to stick together.
Why is the sickle cell allele not eliminated by
natural selection?
Benefit of the allele
Because the sickle cell allele also is beneficial under
certain circumstances.
Only individuals homozygous for sickle cell gene get sickle
cell anemia.
Individuals with one copy of sickle cell gene
(heterozygotes) get sickle cell trait (mild form of disease).
Individuals with sickle cell trait don’t get malaria.
Malaria
Malaria is one of the most important diseases in
the world.
About 500 million cases and an estimated 700,000
to 2.7 million deaths occur worldwide each year
(CDC).
Malaria was well known to the Ancient Greeks
and Romans. The Romans thought the disease
was caused by bad air (in Latin mal-aria) from
swamps, which they drained to prevent the
disease.
Malaria is caused by infection with a single–celled
sporozoan parasite called Plasmodium.
It is transmitted by the bite of an Anopholes
mosquito
Life cycle of Plasmodium
Plasmodium has two hosts: mosquitoes and
humans and a complex life cycle.
Sexual reproduction takes place in the mosquito
and the parasite is transmitted to humans when the
mosquito takes a blood meal.
In a human Plasmodium goes reproduces in liver
cells and then red blood cells before being picked
up by a mosquito to continue the cycle again.
Symptoms
The severity of a malaria infection may range
from asymptomatic (no apparent sign of illness) to
the classic symptoms of malaria (fever, chills,
sweating, headaches, muscle pains), to severe
complications (e.g. anemia, kidney failure) that
can result in death.
Sickle cell allele protects against
malaria
People with the sickle cell allele are protected
against Plasmodium because their hemoglobin
under low oxygen conditions contracts into
needle-shaped clumps.
This contraction not only causes the sickling of the
cell, but harms the parasite. Parasites are impaled
on the clumps and the cell loses its ability to pump
potassium, which the parasite needs.
Heterozygote advantage
Heterozygotes (those with one copy of the sickle cell
allele have higher survival than either homozygote. So called:
“Heterozygote advantage”.
Sickle cell homozygotes die of sickle cell anemia
“Normal” homozygotes more likely to die of malaria.
Thus there is stabilizing selection for sickle cell allele. The
allele is maintained in the population.
Sickle cell allele in African
Americans
Given what you know about the sickle cell
allele, what changes would you expect to
see over time in the frequency of the allele
in African-American populations in the
U.S.?
Natural History of HIV/AIDS
Acquired immune deficiency syndrome (AIDS)
caused by Human Immunodeficiency Virus (HIV).
Immune system attacked. Victim dies of secondary
infections.
Projected mortality by 2020 --90 million lives
Responsible for about 5% of all deaths worldwide.
The Human Immunodeficiency
Virus
HIV, like all viruses, is an intracellular parasite.
Parasitizes macrophages and T-cells of immune
system.
Uses cells enzymatic machinery to copy itself.
Kills host cell in process.
Cells HIV infects are critical to immune system
function.
Immune system collapse leads to AIDS.
Patient vulnerable to opportunistic infections.
Why is HIV hard to treat?
Drug resistance.
AZT (azidothymidine) first HIV wonder
drug
Works by interfering with HIV’s reverse
transcriptase enzyme, which the virus uses
to transcribe its viral RNA into DNA
Drug resistance.
AZT similar to thymidine (one of 4 bases of
DNA nucleotides) but has an azide group
(N3) in place of hydroxyl group (OH).
AZT added to DNA strand prevents strand
from growing. Azide blocks attachment of
next nucleotide.
Drug resistance.
AZT successful in tests although with
serious side effects.
After only a few years patients stopped
responding to treatment.
Evolution of AZT-resistant HIV in patients
usually took only about 6 months.
How does resistant virus differ?
Reverse transcriptase gene in resistant
strains differ genetically from non-resistant
strains.
Mutations located in active site of reverse
transcriptase.
Selectively block binding of AZT
How did resistance develop?
HIV reverse transcriptase very error prone.
Half of DNA transcripts produced contain
an error (mutation).
HIV has highest mutation rate known.
There is thus VARIATION in the HIV
population in a patient.
How did resistance develop?
High mutation rate makes occurrence of
AZT-resistant mutations almost certain.
NATURAL SELECTION now starts to act
in presence of AZT
Selection in action
Presence of AZT suppresses replication of
non-resistant strains.
Resistant strains replicate and pass on their
resistance. Resistance is HERITABLE.
AZT-resistant strains replace non-resistant
strains. EVOLUTION has occurred.
Other examples of natural
selection
There are other examples of natural
selection in action in your textbook chapter
22. You should study these too.