Concept explainers
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
Want to see the full answer?
Check out a sample textbook solutionChapter 23 Solutions
Campbell Biology Plus Mastering Biology with Pearson eText - Access Card Package (11th Edition)
- 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
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education