The mutation causing sickle-cell anemia in humans, which changes the normal T to an A in the sixth codon (substituting valine for glutamic acid), occurs in which gene of the hemoglobin family? the a-globin gene (alpha) the b-globin gene (beta) the g-globin gene (gamma) the d-globin gene (delta) the e-globin gene (epsilon)

The mutation causing sickle-cell anemia in humans, which changes the normal T to an A in the sixth codon (substituting valine for glutamic acid), occurs in which gene of the hemoglobin family? the a-globin gene (alpha) the b-globin gene (beta) the g-globin gene (gamma) the d-globin gene (delta) the e-globin gene (epsilon)

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter10: From Proteins To Phenotypes

Section: Chapter Questions

Problem 20QP: If an extra nucleotide is inserted in the first exon of the beta globin gene, what effect will it...

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Consider the genes that specify the structure of hemoglobin. Arrange the following events in the most likely sequence in which they would take place.a. Anemia is observed.b. The shape of the oxygen-binding site is altered.c. An incorrect codon is transcribed into hemoglobinmRNA.d. The ovum (female gamete) receives a high radiationdose.e. An incorrect codon is generated in the DNA of ahemoglobin gene.f. A mother (an X-ray technician) accidentally stepsin front of an operating X-ray generator.g. A child dies.h. The oxygen-transport capacity of the body is severelyimpaired.i. The tRNA anticodon that lines up is one of a typethat brings an unsuitable amino acid.j. Nucleotide-pair substitution occurs in the DNA of agene for hemoglobin
C5. A human gene called the β-globin gene encodes a polypeptide that functions as a subunit of the protein known as hemoglobin. Hemoglobin is found within red blood cells; it carries oxygen. In human populations, the β-globin gene can be found as the common allele called the HbA allele, and it can also be found as the HbS allele. Individuals who have two copies of the HbS allele have the disease called sickle cell disease. Are the following descriptions examples of genetics at the molecular, cellular, organism, or population level? A. The HbS allele encodes a polypeptide that functions slightly differently from the polypeptide encoded by the HbA allele. B. If an individual has two copies of the HbS allele, that person’s red blood cells take on a sickle cell shape. C. Individuals who have two copies of the HbA allele do not have sickle cell disease, but they are not resistant to malaria. People who have one HbA allele and one HbS allele do not have sickle…
Sickle-cell disease (often called sickle-cell anemia) is a disease that is caused by a mutation to the gene that is responsible for producing the protein hemoglobin. Remember that hemoglobin is a protein in the red blood cells which is responsible for carrying oxygen throughout the body. When a person possesses the mutated hemoglobin allele, their red blood cells take on an altered shape and this results in a variety of symptoms ranging from general weakening of the body, damage to the organs and even death. The sickle cell allele is recessive to the healthy allele, thus only individuals that are homozygous for the recessive allele will have sickle-cell disease. Individuals that are homozygous for the healthy allele, along with heterozygous, individuals will be physically healthy. Question: Given that this mutated allele will cause disease and death in individuals, what would you predict to occur to the frequency of this allele in the population? Explain.
Who Owns Your Genome? John Moore, an engineer working on the Alaska oil pipeline, was diagnosed in the mid-1970s with a rare and fatal form of cancer known as hairy cell leukemia. This disease causes overproduction of one type of white blood cell known as a T lymphocyte. Moore went to the UCLA Medical Center for treatment and was examined by Dr. David Golde, who recommended that Moores spleen be removed in an attempt to slow down or stop the cancer. For the next 8 years, John Moore returned to UCLA for checkups. Unknown to Moore, Dr. Golde and his research assistant applied for and received a patent on a cell line and products of that cell line derived from Moores spleen. The cell line, named Mo, produced a protein that stimulates the growth of two types of blood cells that are important in identifying and killing cancer cells. Arrangements were made with Genetics Institute, a small start-up company, and then Sandoz Pharmaceuticals, to develop the cell line and produce the growth-stimulating protein. Moore found out about the cell line and its related patents and filed suit to claim ownership of his cells and asked for a share of the profits derived from the sale of the cells or products from the cells. Eventually, the case went through three courts, and in July 1990n years after the case beganthe California Supreme Court ruled that patients such as John Moore do not have property rights over any cells or tissues removed from their bodies that are used later to develop drugs or other commercial products. This case was the first in the nation to establish a legal precedent for the commercial development and use of human tissue. The National Organ Transplant Act of 1984 prevents the sale of human organs. Current laws allow the sale of human tissues and cells but do not define ownership interests of donors. Questions originally raised in the Moore case remain largely unresolved in laws and public policy. These questions are being raised in many other cases as well. Who owns fetal and adult stem-cell lines established from donors, and who has ownership of and a commercial interest in diagnostic tests developed through cell and tissue donations by affected individuals? Who benefits from new genetic technologies based on molecules, cells, or tissues contributed by patients? Are these financial, medical, and ethical benefits being distributed fairly? What can be done to ensure that risks and benefits are distributed in an equitable manner? Gaps between technology, laws, and public policy developed with the advent of recombinant DNA technology in the 1970s, and in the intervening decades, those gaps have not been closed. These controversies are likely to continue as new developments in technology continue to outpace social consensus about their use. Should the physicians at UCLA have told Mr. Moore that his cells and its products were being commercially developed?
Who Owns Your Genome? John Moore, an engineer working on the Alaska oil pipeline, was diagnosed in the mid-1970s with a rare and fatal form of cancer known as hairy cell leukemia. This disease causes overproduction of one type of white blood cell known as a T lymphocyte. Moore went to the UCLA Medical Center for treatment and was examined by Dr. David Golde, who recommended that Moores spleen be removed in an attempt to slow down or stop the cancer. For the next 8 years, John Moore returned to UCLA for checkups. Unknown to Moore, Dr. Golde and his research assistant applied for and received a patent on a cell line and products of that cell line derived from Moores spleen. The cell line, named Mo, produced a protein that stimulates the growth of two types of blood cells that are important in identifying and killing cancer cells. Arrangements were made with Genetics Institute, a small start-up company, and then Sandoz Pharmaceuticals, to develop the cell line and produce the growth-stimulating protein. Moore found out about the cell line and its related patents and filed suit to claim ownership of his cells and asked for a share of the profits derived from the sale of the cells or products from the cells. Eventually, the case went through three courts, and in July 1990n years after the case beganthe California Supreme Court ruled that patients such as John Moore do not have property rights over any cells or tissues removed from their bodies that are used later to develop drugs or other commercial products. This case was the first in the nation to establish a legal precedent for the commercial development and use of human tissue. The National Organ Transplant Act of 1984 prevents the sale of human organs. Current laws allow the sale of human tissues and cells but do not define ownership interests of donors. Questions originally raised in the Moore case remain largely unresolved in laws and public policy. These questions are being raised in many other cases as well. Who owns fetal and adult stem-cell lines established from donors, and who has ownership of and a commercial interest in diagnostic tests developed through cell and tissue donations by affected individuals? Who benefits from new genetic technologies based on molecules, cells, or tissues contributed by patients? Are these financial, medical, and ethical benefits being distributed fairly? What can be done to ensure that risks and benefits are distributed in an equitable manner? Gaps between technology, laws, and public policy developed with the advent of recombinant DNA technology in the 1970s, and in the intervening decades, those gaps have not been closed. These controversies are likely to continue as new developments in technology continue to outpace social consensus about their use. Do you think that donors or patients who provide cells and/or tissues should retain ownership of their body parts or should share in any financial benefits that might derive from their use in research or commercial applications?
Beadle and Tatum's experiments led to the "one gene - one enzyme (protein)" hypothesis. In subsequent years, many exceptions to this hypothesis were noted. A molecule of hemoglobin fails to support this hypothesis for which of the following reasons? n eukaryotes, one gene can code form multiple isoforms of a polypeptide. The functional hemoglobin protein is made from multiple polypeptides. Not all enzymes are proteins. Not all genes encode proteins.
The genetic alteration responsible for sickle-cell anemia in humans involves: a transition mutation from A to G, substituting glutamic acid for valine in a-globin a transversion mutation from T to A, substituting valine for glutamic acid in b-globin a transition mutation from T to C, substituting valine for glutamic acid in b-globin a transversion mutation from G to C, substituting glutamic acid for valine in a-globin a frameshift mutation of one ATC codon, removing glutamic acid from b-globin
A molecular geneticist hopes to find a Gene in human liver cell that codes for an important blood-clotting protein,he knows that the nucleotide sequence of a small part of the Gene is GTGGACTGACA.briefly explain how to obtain gene
Define a Point mutation and give an example. What is sickle cell anemia and what causes it. What is nondisjunction? How does nondisjunction cause disorders? NUMER YOUR ANSWERS
Why is gene duplication within globin genes beneficial?
One of your patients, a six-year-old girl who suffers from Sickle cell anemia, an inherited blood disorder in which red blood cells are abnormally shaped and fragile, leading to a short supply of red blood cells. These abnormal cells can also get stuck in small vessels, which prevent blood flow, leading to fatigue, pain, and other severe complications. Patients with sickle cell anemia produce defective beta-globin due to a point mutation that causes the change of a single amino acid residue. This is an example of what type of mutation? nonsense mutation missense mutation frameshift mutation deletion mutation
Using sickle-cell anemia as an example, describe what is meant by a molecular or genetic disease. What are the similarities and dissimilarities between this type of a disorder and a disease caused by an invading microorganism?