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Examples of Natural Selection in action Peppered Moth Darwin’s Finches on Daphne major Sickle Cell Anemia and Malaria HIV and drug resistance.

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Presentation on theme: "Examples of Natural Selection in action Peppered Moth Darwin’s Finches on Daphne major Sickle Cell Anemia and Malaria HIV and drug resistance."— Presentation transcript:

1 Examples of Natural Selection in action Peppered Moth Darwin’s Finches on Daphne major Sickle Cell Anemia and Malaria HIV and drug resistance

2 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.

3 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).

4 Peppered moths rest on trees and depend on camouflage for protection.

5 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.


7 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.


9 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.

10 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.

11 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.

12 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.


14 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.


16 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.


18 Why is the sickle cell allele not eliminated by natural selection?

19 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.

20 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.

21 Malaria is caused by infection with a single–celled sporozoan parasite called Plasmodium. It is transmitted by the bite of an Anopholes mosquito


23 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.


25 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.

26 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.


28 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.

29 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.?


31 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.

32 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.


34 Cells HIV infects are critical to immune system function. Immune system collapse leads to AIDS. Patient vulnerable to opportunistic infections.

35 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

36 Drug resistance. AZT similar to thymidine (one of 4 bases of DNA nucleotides) but has an azide group (N 3 ) in place of hydroxyl group (OH). AZT added to DNA strand prevents strand from growing. Azide blocks attachment of next nucleotide.


38 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.


40 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


42 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.

43 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


45 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.

46 Other examples of natural selection There are other examples of natural selection in action in your textbook chapter 22. You should study these too.

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