How would present allele frequencies of the sickle cell allele change, if there was no heterozygote advantage or disadvantage (that is, that heterozygotes would be identical to ‘normal’ homozygotes – no malaria resistance, no anemia)? How would the change in sickle cell allele frequencies compare to scenario a (extirpation of malaria)

How would present allele frequencies of the sickle cell allele change, if there was no heterozygote advantage or disadvantage (that is, that heterozygotes would be identical to ‘normal’ homozygotes – no malaria resistance, no anemia)? How would the change in sickle cell allele frequencies compare to scenario a (extirpation of malaria)

Human Biology (MindTap Course List)

11th Edition

ISBN:9781305112100

Author:Cecie Starr, Beverly McMillan

Publisher:Cecie Starr, Beverly McMillan

Chapter19: Introduction To Genetics

Section: Chapter Questions

Problem 9CT

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The allele of the gene responsible for the lung disorder, cystic fibrosis rose to prominence in Europe in the 1800s. Cystic fibrosis disease results from thick mucus accumulating in the lungs, which occurs in individuals who are homozygous for the CF allele. A pleiotropic effect is that heterozygous individuals are less likely to suffer from diarrhea. During the European cholera epidemics of the 1800s, resistance against diarrhea conferred a survival advantage such that approximately one in every 400 people in some European populations have cystic fibrosis. Fill in the table below with the genotype and allele frequencies for this 1 in 400 occurrence and provide the Hardy-Weinberg principle model you will be using. (Assume that individuals with the cystic fibrosis trait (CF) reproduce normally and that good sanitation means that there is currently no fitness advantage to diarrhea resistance.) phenotype CF DR normal (totals) Genotype cc Cc CC Number of Individuals 1 ______…
Take the example of B-thalassemia, an autosomal recessive genetic disease that particularly affects people from around the Mediterranean. This disease is associated with an anomaly of hemoglobin, a protein essential for the transport of oxygen, which is composed of four chains: two alpha (a) and two beta (B). In case of B-thalassemia, the ẞ chains are produced in insufficient or no quantity in an individual homozygous recessive resulting in insufficient production of overall hemoglobin leading to anemia and other physiological challenges. The gene that controls the synthesis of the ẞ chains is located on chromosome 11. Here is part of the coding portion of this gene (which controls a total of 146 amino acids and of which you only see the portion 36 to 41) and one of the targeted mutations: 1. Give the sequence of amino acids from the template and mutated strands. 2. What type of point mutation is it? 3. Using the principles of the theory of evolution, explain briefly and generally why…
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of this genetic defect causes deformation of red blood cells. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. Assuming HWE, if 9% of an African population is born with a severe form of sickle-cell anemia (ss), what percentage of the population will be more resistant to malaria…
One particularly useful feature of the Hardy-Weinberg equation is that it allows us to estimate the frequency of heterozygotes for recessive genetic diseases, assuming that Hardy-Weinberg equilibrium exists. As an example, let’s consider cystic fibrosis, which is a human genetic disease involving a gene that encodes a chloride transporter. Persons with this disorder have an irregularity in salt and water balance. One of the symptoms is thick mucus in the lungs that can contribute to repeated lung infections. In populations of Northern European descent, the frequency of affected individuals is approximately 1 in 2500. Because this is a recessive disorder, affected individuals are homozygotes. Assuming that the population is in Hardy-Weinberg equilibrium, what is the frequency of individuals who are heterozygous carriers?
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of the genetic defect. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. 11% of an African 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…
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of the genetic defect. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. 11% of an African population is born with a severe form of sickle-cell anemia (ss), What is the frequency of the dominant allele? Please show your work in order to receive credit.
Sickle-cell anemia is an interesting genetic disease. Normal homozygous individials (SS) have normal blood cells that are easily infected with the malarial parasite. Thus, many of these individuals become very ill from the parasite and many die. Individuals homozygous for the sickle-cell trait (ss) have red blood cells that readily collapse when deoxygenated. Although malaria cannot grow in these red blood cells, individuals often die because of the genetic defect. However, individuals with the heterozygous condition (Ss) have some sickling of red blood cells, but generally not enough to cause mortality. In addition, malaria cannot survive well within these "partially defective" red blood cells. Thus, heterozygotes tend to survive better than either of the homozygous conditions. 11% of an African population is born with a severe form of sickle-cell anemia (ss), What is the frequency of the recessive allele? Please show your work in order
A research team genotyped hundreds of families affected by haemophilia. Among those families, they found many that had a pattern of RFLP like that of daughter1, her husband and her parents. When they genotyped the children in those families, they found the following association between the RFLP and hemophilia: The numbers at the bottom indicate the number of progeny with that combination of hemophilia phenotype and RFLP polymorphism found among these families. What is the map distance between the RFLP and the hemophilia gene? Show your work.
Cystic fibrosis (CF) is an autosomal recessive trait. A three-generation pedigree is shown below for a family that carries the mutant allele for cystic fibrosis. Note that carriers are not colored in to allow you to figure out their genotypes. Normal allele = F CF mutant allele = f What is the genotype of individual #13? A) ff B) FF C) Ff D) it is impossible to tell
A mutant allele in persons with familial hypercholesterolemia (FH) causes death due to a lack of liver receptors for LDL. Susceptible persons have half the normal number of receptors, while other individuals have the normal number of receptors. In a phenotypically normal couple, the man had a female 1 cousin (on his father’s side) who died from FH; the woman had a maternal uncle with FH. Using standard symbols, draw apedigree of these couple’s families. Write the genotypes of each family member.
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Below in Figure 1 is a pedigree for a family afflicted by a genetic disorder. In some populations, Cystic fibrosis has an incidence of 1 in 2500 newborns. The carrier frequency calculated from this is 1/25. Analyze the pedigree below assuming the disease is similar to cystic fibrosis in incidence and carrier frequency. However this disease may not have the same type of genetic transmission as cystic fibrosis. What type of genetic transmission is most consistent with the pedigree? Label all the individuals that you can determine, with hypothesized genotypes. Label the individuals that have unknown genotypes with possible genotypes. Assuming her father is known to NOT be a carrier, calculate the probability that IV1 is a carrier for disease. Use the Χ2 test to determine whether your proposed transmission fits this data.