Concept explainers
To analyze:
Nine base pair deletion in the genome of mitochondria between the cytochrome oxidase subunit II gene and
Introduction:
The examination of variations in genome of mitochondria in human populations gives us an idea about the journey of human ancestors throughout the world (out of Africa).The variation pattern of mitochondrial DNA indicates the African origin and journey of modern humans throughout the world.
Want to see the full answer?
Check out a sample textbook solutionChapter D Solutions
Genetic Analysis: An Integrated Approach Plus Mastering Genetics with Pearson eText -- Access Card Package (3rd Edition) (What's New in Genetics)
- Sickle-cell anemia is a recessive autosomal disorderthat is caused by an amino acid substitution in theβ-hemoglobin protein. The DNA mutation underlyingthis substitution is a SNP that alters a GAG codon forthe amino acid glutamate to a GTG that codes a valine.The frequency of sickle-cell anemia among AfricanAmericans is about 1/400. What is the frequency ofthis GTG codon in the β-hemoglobin gene amongAfrican Americans?arrow_forwardThe 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_forwardIf you compare the frequency of the sixteen possible dinucleotide sequences in the E. coli and human genomes, there are no striking differences except for one dinucleotide, 5ʹ-CG-3ʹ. The frequency of CG dinucleotides in the human genome is significantly lower than in E. coli and significantly lower than expected by chance. Why do you suppose that CG dinucleotides are underrepresented in the human genome? (hint: The C in the CG pair is often methylated). Explain how this observation has an impact on the cells immune response.arrow_forward
- The HbβS(sickle-cell) allele of the human β-globingene changes the sixth amino acid in the β-globinchain from glutamic acid to valine. In HbβC, the sixthamino acid in β-globin is changed from glutamic acidto lysine. What would be the order of these two mutations within the map of the β-globin gene?arrow_forward54. 35delG mutation in the connexin 26 gene is an autosomal recessive condition that has been identified to cause congenital deafness. In a population of 367 Greek children, 75 of the children carried two copies of the 35delG mutation.In order to calculate the percentage of individuals who are heterozygous for the 35delG mutation, the calculation that must be performed is Select one: a. 1 – (p2 – 2pq) b. 1 – (p +q) c. 1 – (p2 + q2) d. 1 – q2arrow_forwardMitochondrial DNA sequences have been detected in the nuclear genomes of many organisms, and cpDNA sequences are sometimes found in the mitochondrial genome. Propose a mechanism for how such “promiscuous DNA” might move between nuclear, mitochondrial, and chloroplast genomes.arrow_forward
- Fig 2 shows gastric organoids cultured from a TffCre; XYZI/fl mouse. Ki67 has been used to identify proliferating cells (green). Tamoxifen indicates exposure to tamoxifen to induce recombination of the TffCre. No Tamoxifen Ki-67 3. What is the consequence of deleting XYZ in gastric organoids, and does this suggest it is an oncogene or a tumour suppressor? Explain your reasoning. DX Equation Editor 4. IWP inhibits the secretion of Wnt ligands from the organoids. Therefore, do Wnt ligands promote or inhibit proliferation of XYZ deficient organoids? Explain your reasoning. X Equation Editor Tamoxifen Q Tamoxifen + IWP A- A I B IU S x, x² Styles Font Size Font Words: 0/250 张 A- A-T BIUS X, x² Styles ▾ Sizearrow_forwardTHE MOLECULAR GENETICS OF CYSTIC FIBROSIS and of The following is the base sequence of DNA that codes for amino acids 506-510 of the protein that regulates the chlorine channels in the cell membrane. This protein contains a total of 1476 amino acids so this is a small part of the entire gene. DNA Template Strand: 3'TAGTAGAAACCACAA5' 1. What is the minimum number of DNA nucleotides in this whole gene? 2. What is the sequence of bases on the strand of DNA that is complementary to the template strand? 3. What mRNA will be formed from the template strand of DNA? 4. What amino acids will this mRNA code for? 5. If the 6th, 7th and 8th bases in the template strand of the DNA are removed, rewrite the new template strand below. 6. When the template strand of the DNA is changed, this is referred to as a mutation. What kind of mutation is this? 65arrow_forwardPeople who carry a theoretical genetic disorder (called B-disease) can be identified from a 2kb DNA sequence. People who carry this genetic disorder have a single nucleotide polymorphism that results in a change of GTATCC to GGATCC, a site that only occurs once at nucleotide number 750 in this DNA sequence. Answer the following questions based on the information provided. (a) How can you develop a simple molecular test to identify the genetic disorder?r B-dif w. (41 (b) If you have carried out the molecular test (based on the information above) on a 100 individual and found that 24 were healthy (BB) and 26 were carriers (bb); 1) What is the ratio of heterozygous? 2) Show how can you identify the three types from the agarose gel (H focaiarrow_forward
- Diamond–Blackfan anemia (DBA) is a rare, dominantgenetic disorder characterized by bone marrow malfunction,birth defects, and a predisposition to certaincancers. Infants with DBA usually develop anemia in the firstyear of life, have lower than normal production of red blood cellsin their bone marrow, and have a high risk of developing leukemiaand bone cancer. At the molecular level, DBA is causedby mutations in any one of 10 genes that encode ribosomalproteins. The first-line therapy for DBA is steroid treatment,but more than half of affected children develop resistance tothe drugs and in these cases, treatment is halted. DBA can betreated successfully with bone marrow or stem cell transplantsfrom donors with closely matching immune system markers.Transplants from unrelated donors have significant levels ofcomplications and mortality. While a stem cell transplant from an unaffected donor is currentlythe only cure for DBA, genome-editing technologies mayone day enable the correction of…arrow_forwardDiamond–Blackfan anemia (DBA) is a rare, dominantgenetic disorder characterized by bone marrow malfunction,birth defects, and a predisposition to certaincancers. Infants with DBA usually develop anemia in the firstyear of life, have lower than normal production of red blood cellsin their bone marrow, and have a high risk of developing leukemiaand bone cancer. At the molecular level, DBA is causedby mutations in any one of 10 genes that encode ribosomalproteins. The first-line therapy for DBA is steroid treatment,but more than half of affected children develop resistance tothe drugs and in these cases, treatment is halted. DBA can betreated successfully with bone marrow or stem cell transplantsfrom donors with closely matching immune system markers.Transplants from unrelated donors have significant levels ofcomplications and mortality. Given that a faulty ribosomal protein is the culprit and causesDBA, discuss the possible role of normal ribosomal proteins.Why might bone marrow cells be…arrow_forwardLeber Congenital Amaurosis (LCA) causes progressive vision loss due to defects in the gene that encodes RPE65 isomerase. Affected individuals are homozygous recessive for mutant alleles of the RPE65 gene. You are trying to determine the molecular nature of the mutations in three individuals with LCA. For ease of analysis, you may assume that each individual is homozygous for the same mutant allele (though the three individuals have different mutations than each other). You use the polymerase chain reaction to amplify DNA from each patient and you determine the sequence of the DNA and compare it to unaffected individuals. You identify the following differences. Note that the non-template strand of DNA is given and the changes are highlighted using red boldface. You can assume that the sequences are in the first reading frame (eg. the first three nucleotides of each sequence is a codon). The coding region of the gene is 1602 bp and the position of the sequences shown below is…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