19) Thalassaemia is a genetic disorder in which the red blood cells in the body cannot carryoxygen. A mutation in the thalassaemia gene prevents hemoglobin, the protein responsible forcarrying oxygen around the body, from carrying a lot of oxygen. This makes people withthalassaemia very tired and they have a lot of trouble breathing.A. Look at the DNA sequences for normal hemoglobin and the mutated form of hemoglobin.Fill in the chart to find the mRNA, and the amino acid sequence for the mutated DNA.Normal HemoglobinDNA SequenceCC TTG |GACCCAGAG GTTCMRNA|C |C|UUG|G|ACCCAGAG G|UUCAmino AcidsPROTRPTHRGLNARGPHEMutated HemoglobinCodons Found in Messenger RNASecond BaseDNA SequenceCCTT|G G|ACCTAGUCA GPheSerSerSerTyrTyrStopCys UСуsStopGPheULeuLeuSerStopTrpArgmRNALeuProHisLeuCLeuProHisArgАrgArgProGinLeuProGinAmino AcidsleThrAsnSerUAleThrAsnSerleThrLysArgMetThrLysAspArgGlyValAlaB. Explain the difference between the normal and mutated formsof hemoglobin. What type of mutation occurred? Predict whythis mutation prevents hemoglobin from working correctly.UGlyAValGAlaAlaAlaАврGluGluGlyGValValGlyThird Base

19) Thalassaemia is a genetic disorder in which the red blood cells in the body cannot carry oxygen. A mutation in the thalassaemia gene prevents hemoglobin, the protein responsible for carrying oxygen around the body, from carrying a lot of oxygen. This makes people with thalassaemia very tired and they have a lot of trouble breathing. A. Look at the DNA sequences for normal hemoglobin and the mutated form of hemoglobin. Fill in the chart to find the mRNA, and the amino acid sequence for the mutated DNA. Normal Hemoglobin DNA Sequence CCTTGGACCCAGAGGTTC |c CUUGGACCCAGAGGUUC mRNA Amino Acids THR PRO TRP GLN ARG PHE Mutated Hemoglobin Codons Found in Messenger RNA Second Base UCAG Cys u Cys c Stop A Trp Arg Arg Arg Arg DNA Sequence CCTTGG |ACCTAG Ser Ser Phe Tyr Tyr Phe Leu Ser Ser Stop Stop Leu MRNA Leu Pro His Leu Pro His C Leu Pro Gin Leu Pro Gih Amino Acids le Thr Asn Ser A le Thr Asn Ser le Thr Lys Arg A. Met The Lys Arg Gly C Val Ala B. Explain the difference between the normal and mutated forms of hemoglobin. What type of mutation occurred? Predict why this mutation prevents hemoglobin from working correctly. Asp Asp Glu Ala Gly Gly G Val Val Ala Val Ala Glu Gly irst Base Third Base

19) Thalassaemia is a genetic disorder in which the red blood cells in the body cannot carry oxygen. A mutation in the thalassaemia gene prevents hemoglobin, the protein responsible for carrying oxygen around the body, from carrying a lot of oxygen. This makes people with thalassaemia very tired and they have a lot of trouble breathing. A. Look at the DNA sequences for normal hemoglobin and the mutated form of hemoglobin. Fill in the chart to find the mRNA, and the amino acid sequence for the mutated DNA. Normal Hemoglobin DNA Sequence CCTTGGACCCAGAGGTTC |c CUUGGACCCAGAGGUUC mRNA Amino Acids THR PRO TRP GLN ARG PHE Mutated Hemoglobin Codons Found in Messenger RNA Second Base UCAG Cys u Cys c Stop A Trp Arg Arg Arg Arg DNA Sequence CCTTGG |ACCTAG Ser Ser Phe Tyr Tyr Phe Leu Ser Ser Stop Stop Leu MRNA Leu Pro His Leu Pro His C Leu Pro Gin Leu Pro Gih Amino Acids le Thr Asn Ser A le Thr Asn Ser le Thr Lys Arg A. Met The Lys Arg Gly C Val Ala B. Explain the difference between the normal and mutated forms of hemoglobin. What type of mutation occurred? Predict why this mutation prevents hemoglobin from working correctly. Asp Asp Glu Ala Gly Gly G Val Val Ala Val Ala Glu Gly irst Base Third Base

Biology (MindTap Course List)

11th Edition

ISBN:9781337392938

Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Publisher:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg

Chapter16: Human Genetics And The Human Genome

Section: Chapter Questions

Problem 6TYU

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a. Which gene is mutated in individuals with sickle-cell anemia? b. What are the major symptoms of this disorder? c. What was the first published scientific description of sickle-cell anemia? d. Describe two other features of this disorder that you learned from the OMIM database and state where in the database you found this information
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…
2 I 3 4 5 6 I 7 Sickle cell hemoglobin DNA CACGTAGACTGAGGACAC.. sheet: Deletio... obin DNA C A... globin DNA C... Sickle cell hemoglobin mRNA: Sickle cell hemoglobin Amino Acid sequence: 4. What type of mutation is this? Please explain why.
Determine which statements could be used as evidence to support the argument that "DNA influences the proteins that are made" and which statements are just facts. [Select all that apply.] The HBB gene that makes beta-globin has several abnormal alleles, including HbS, HbC, and HbE. Sickle cell disease has been successfully treated using bone marrow transplantation in children and adults. The symptoms of sickle cell anemia may not appear in individuals who only carry one HbS allele, but are always apparent when both alleles are HbS. If oxygen is removed from red blood cells made by two HbS alleles, the cell will form a sickle shape.
Which of the given disorder can be seen in an individual when the mutation includes substitution of a purine by pyrimidine? 1. Chronic myelogenous leukemia 2. Sickle cell anaemia 3. a thalassemia 4. B thalassemia
. 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)
1. A monogenic disease is a disease caused by a mutation in a single gene. For instance, sickle-cell anemia is caused by a mutation in the HBB gene, which codes for the B- globin chain of hemoglobin. The beginning of HBB is shown here: 5'-ATGGTGCACCTGACTCCTGAGGAGAAGTCTGCCGTTACT...-3' A. Translate this HBB sequence into an amino acid sequence. B. In terms of amino acids, what is the result of the sickle cell mutation, wherein the bolded red A is changed to a T? This single mutation causes hemoglobin to aggregate, causing red blood cells to deform into a sickle-like shape rather than the normal “biconcave disk" shape. C. What would happen if the bolded blue A were mutated to at T? (This is hypothetical; it's not a mutation found in sickle-cell disease.)
A 30 - year - old woman was undergoing therapy for b-thalassemia,a recessive trait caused by absence of or reduced synthesis ofthe hemoglobin b chain, a subunit of the oxygen-carrying moleculein red blood cells. In this condition, red blood cells are rapidlydestroyed, freeing a large amount of iron, which is deposited in tissuesand organs. The blood transfusions the patient had received every twoor three weeks since the age of 7 to stave off anemia were furtheraggravating iron buildup. Her major organs were showing damage, andshe was in danger of death from cardiac disease. Her physician suggestedthat she consider undergoing a hematopoietic (bone marrow)stem cell transplant (HSCT). Since these stem cells give rise to redblood cells, such a transplant could potentially restore her health. Whilethis might seem like an easy decision, it is not. Advanced cases havea high risk (almost 30 percent) for transplantation-related death. At thispoint, the woman is faced with a difficult and…
. Identify the polypeptide that is found with a-globin in human fetal hemoglobin (first appearing in the late Jurassic, about 145 million years ago, with the origin of placental mammals from marsupials). e-globin (epsilon) g-globin (gamma) d-globin (delta) b-globin (beta) z-globin (zeta)
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
A 30 - year - old woman was undergoing therapy for b-thalassemia,a recessive trait caused by absence of or reduced synthesis ofthe hemoglobin b chain, a subunit of the oxygen-carrying moleculein red blood cells. In this condition, red blood cells are rapidlydestroyed, freeing a large amount of iron, which is deposited in tissuesand organs. The blood transfusions the patient had received every twoor three weeks since the age of 7 to stave off anemia were furtheraggravating iron buildup. Her major organs were showing damage, andshe was in danger of death from cardiac disease. Her physician suggestedthat she consider undergoing a hematopoietic (bone marrow)stem cell transplant (HSCT). Since these stem cells give rise to redblood cells, such a transplant could potentially restore her health. Whilethis might seem like an easy decision, it is not. Advanced cases havea high risk (almost 30 percent) for transplantation-related death. At thispoint, the woman is faced with a difficult and…
. Mutations in an autosomal gene in humans cause aform of hemophilia called von Willebrand disease(vWD). This gene specifies a blood plasma proteincleverly called von Willebrand factor (vWF). vWFstabilizes factor VIII, a blood plasma protein specified by the wild-type hemophilia A gene. Factor VIIIis needed to form blood clots. Thus, factor VIII is rapidly destroyed in the absence of vWF.Which of the following might successfully be employed in the treatment of bleeding episodes in hemophiliac patients? Would the treatments workimmediately or only after some delay needed forprotein synthesis? Would the treatments have only ashort-term or a prolonged effect? Assume that allmutations are null (that is, the mutations result in thecomplete absence of the protein encoded by the gene)and that the plasma is cell-free.a. transfusion of plasma from normal blood into avWD patientb. transfusion of plasma from a vWD patient into adifferent vWD patientc. transfusion of plasma from a hemophilia A…