CAMPBELL BIOLOGY (LL) >CUSTOM PKG.<
17th Edition
ISBN: 9781323745618
Author: Central Texas
Publisher: PEARSON C
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Chapter 23, Problem 8TYU
Summary Introduction
To write: A short essay to explain the molecular and cellular events leading to the heterozygotes individuals in sickle cell trait leading to the individual and population levels of biological organisation. .
Introduction:
Sickle cell disease is the most commonly occurring recessive inherited disorder found in African – Americans with an incidence of 1/400 and a carrier frequency of 1/10. It is caused due to the sickle cell allele that results in the structural and functional abnormality in normal haemoglobin. A point mutation that causes the substitution of glutamic acid by valine at 6th position of β-globin chain of haemoglobin is the main cause. The homozygous recessive individuals suffer severely from the disease; however the heterozygous carriers have the benefit of killing the malarial parasites in malaria rich regions of the World.
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Match the numbered concepts to the lettered facts. Explain why each pair is the best match.
(1) Gene Duplication (2) Molecular Clock (3) Pseudogene (4) SINES and LINES a. Different kinds of globin chains arose over time including myoglobin, alpha globin, beta globin 1, delta globin, and beta globin 2.b. The two human beta globin genes, 1 and 2, differ at 20 base pair sites; only beta gene 1 produces a functional protein.c. In human hemoglobin, the delta polypeptide chain differs by 39 amino acid sites vs. the beta chain.d. The human alpha globin gene and the mouse alpha globin gene are orthologous to each other.
Which of the following proteins is thought to have been the first to evolve from an ancestral gene duplication of the most ancient O2 transporting protein in vertebrate hemoglobin (found today in all vertebrates except the agnathan fishes)?
A. gamma-globin (-globin)
B. epsilon-globin (-globin)
C. alpha-globin (-globin)
D. delta-globin (-globin)
E. zeta-globin (-globin)
What are molecular homologies used for ? Answe in simple terms
Chapter 23 Solutions
CAMPBELL BIOLOGY (LL) >CUSTOM PKG.<
Ch. 23.1 - Explain why genetic Variation within a population...Ch. 23.1 - Ot all the mutations that occur in a population,...Ch. 23.1 - MAKE CONNECTIONS If a population stopped...Ch. 23.2 - A population has 700 individuals, 85 of genotype...Ch. 23.2 - The frequency of allele a is 0.45 for a population...Ch. 23.2 - WHAT IF? A locus that affects susceptibility to a...Ch. 23.3 - In what sense is natural selection more...Ch. 23.3 - Distinguish genetic draft from gene flow in terms...Ch. 23.3 - WH AT IF? Suppose two plant populations exchange...Ch. 23.4 - What is the relative fitness of a sterile mule?...
Ch. 23.4 - Explain why natural selection is the only...Ch. 23.4 - Prob. 3CCCh. 23 - Typically. most of the nucleotide variabillity...Ch. 23 - Is it circular reasoning to calculate p ond q from...Ch. 23 - Would two small, geographically isolated...Ch. 23 - How might secondary sex characteristics in males...Ch. 23 - Natural selection changes allele frequencies...Ch. 23 - Prob. 2TYUCh. 23 - Prob. 3TYUCh. 23 - There are 25 individuals in population 1, all with...Ch. 23 - Prob. 5TYUCh. 23 - EVOLUTION CONNECTION Using at least two examples,...Ch. 23 - SCIENTIFIC INQUIRY INTERPRET THE DATA Researchers...Ch. 23 - Prob. 8TYUCh. 23 - SYNTHESI2E YOUR KNOWLEDGE This kettle lake forracd...
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- The most common allele of the β chain of hemoglobin in humans, ???,HbA, has glutamic acid at the sixth position. Two different amino acid substitutions at the sixth position produce two variants, ???HbS and ???,HbC, of the sickle‑cell allele. The ???HbS allele occurs when valine is substituted for glutamic acid, and the ???HbC allele occurs when lysine is substituted for glutamic acid. To answer the question, refer to the amino acid table. Match the class of amino acid and the chemical property to each possible amino acid. Not all answers will be placed.arrow_forwardExplain the biochemistry behind human blood ABO-type groups. Why is it important to know the blood type first before blood transfusion? What happens when blood types are incompatible?arrow_forwardIf the same portion of the amino acid sequence for turkey hemoglobin was included, who do you think it would have the least differences with, the human, gorilla,horse,kangaroo, or chicken? Why do you think so?arrow_forward
- In a region of Africa, where malaria is prevalent, 40% of the population are found to have sickle-cell anemia. The disease is caused by an abnormal hemoglobin that is found in both homozygotes (S2S2) and heterozygotes (S1S2). Many homozygotes (S2S2) suffer from anemia and often die. Heterozygotes (S1S2) incur a much less debilitating malady called "sickling trait". Approximately 3% of the people with abnormal hemoglobin are homozygotes (1.2\% of the entire population). The fitness of the S2S2 homozygotes is only 1/4 that of the heterozygotes. Where malaria is prevalent, heterozygotes exhibit overdominance with respect to fitness. How would you calculate relative fitness of the S1S1 homozygotes if you're assuming the population is at an equilibrium frequency for S2?arrow_forwardIn recent years, the country of Zambia in Africa has had increasing cases of malaria. If 8 % of the population is born with a severe form of sickle-cell anemia (ss), what percentage of the population will be more resistant to malaria because they are heterozygous (Ss) for the sickle-cell gene, under the Hardy-Weinberg assumption?arrow_forwardCompare molar theories to molecular theories of matching. Please explain and give points.arrow_forward
- In a study of a muscle disorder, several affected families exhibited vision problems, muscle weakness, and deafness (M. Zeviani et al. 1990. American Journal of Human Genetics 47:904–914). Analysis of the mtDNA from affected members of these families revealed that large numbers of their mtDNA molecules possessed deletions of varying lengths. Different members of the same family and even different mitochondria from the same person possessed deletions of different sizes, so the underlying defect appeared to be a tendency for the mtDNA of affected persons to have deletions. A pedigree of one of the families studied is shown below. The researchers concluded that this disorder is inherited as an autosomal dominant trait, and they mapped the diseasecausing gene to a position on chromosome 10 in the nucleus. Q. What characteristics of the pedigree rule out inheritance of a trait encoded by a gene in the mtDNA as the cause of this disorder?arrow_forwardIn a study of a muscle disorder, several affected families exhibited vision problems, muscle weakness, and deafness (M. Zeviani et al. 1990. American Journal of Human Genetics 47:904–914). Analysis of the mtDNA from affected members of these families revealed that large numbers of their mtDNA molecules possessed deletions of varying lengths. Different members of the same family and even different mitochondria from the same person possessed deletions of different sizes, so the underlying defect appeared to be a tendency for the mtDNA of affected persons to have deletions. A pedigree of one of the families studied is shown below. The researchers concluded that this disorder is inherited as an autosomal dominant trait, and they mapped the diseasecausing gene to a position on chromosome 10 in the nucleus. Q. Explain how a mutation in a nuclear gene might lead to deletions in mtDNA.arrow_forwardAlpha thalassemia is a hereditary blood condition that results in varying levels of anemia. It is tied to the HB alpha 1 gene and the HB alpha 2 gene on human chromosome 16. The diagram shows the proteins for the hemoglobin genes and the pedigree shows genotypes, designated by the letter X, on the chromosomes for a family affected by the condition. Which represents the predicted level of anemia in a child born to the mother and father in the image with a mutation that results in a genotype of xxxx? Why? A - mild anemia because the loss of 4 genes would equal the loss of the 4 proteins needed for normal alpha hemoglobin B - severe anemia because the loss of 4 genes would equal the loss of the 4 proteins needed for normal alpha hemoglobin C - mild anemia because the addition of 4 genes would produce too many of the proteins needed for normal alpha hemoglobin D - severe anemia because the addition of 4 genes would produce too many of the proteins needed for normal alpha hemoglobinarrow_forward
- Explain the differences between an individual homozygous for the sickle hemoglobin allele (HbS/HbS) and one who is heterozygous (HbA/HbS). Consider the hemoglobin molecule, cells, and disease.arrow_forwardFor Mole Faction why do you sum T + C = 1 - A - G? Where did the 1 come from? What does it mean? Also if the mole fraction for A is 0.22 where do you get 20% from?arrow_forwardExplain the graph. What are represented by the red and green lines?arrow_forward
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