17. The effect sizes for the SNPS linked to performance on IQ tests are very very small. Why does that make it unlikely that we can genetically engineer humans with super high IQ? 18. True or False: Diseases such as type II diabetes and lung cancer are likely caused by mutations to a single gene. Explain your answer. 19. True or False: SNPS that are associated to disease using GWAS design should be immediately consid- ered for further molecular functional studies. Explain your answer.

17. The effect sizes for the SNPS linked to performance on IQ tests are very very small. Why does that make it unlikely that we can genetically engineer humans with super high IQ? 18. True or False: Diseases such as type II diabetes and lung cancer are likely caused by mutations to a single gene. Explain your answer. 19. True or False: SNPS that are associated to disease using GWAS design should be immediately consid- ered for further molecular functional studies. Explain your answer.

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Description: 17. The effect sizes for the SNPS linked to performance on IQ tests are very very small. Why does that makeit unlikely that we can genetically engineer humans with super high IQ?18. True or False: Diseases such as type II diabetes and lung cancer ar

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter8: The Structure, Replication, And Chromosomal Organization Of Dna

Section8.4: The Watson-crick Model Of Dna Structure

Problem 2GR

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Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand thecause of the aberrant phenotypes and develop newtherapeutic measures. However, such mice are not always as useful to investigators as it might seem at firstglance. Suppose that you have a mouse knockoutmodel for a human disease caused by homozygosityfor a null allele of a gene. Discuss how the followingsituations might complicate investigations of the human disease based on this mouse model.a. Mice have a shorter life span than humans.b. Mice homozygous for certain knockout mutationsdie in utero.c. Mouse genomes may have additional copies of thegene whose mutation causes the disease in humans.
Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand thecause of the aberrant phenotypes and develop newtherapeutic measures. However, such mice are not always as useful to investigators as it might seem at firstglance. Suppose that you have a mouse knockoutmodel for a human disease caused by homozygosityfor a null allele of a gene. Discuss how the followingsituations might complicate investigations of the human disease based on this mouse model.a. Mice have a shorter life span than humans.b. Mice homozygous for certain knockout mutationsdie in utero.c. Mouse genomes may have additional copies of thegene whose mutation causes the disease in humans.d. Mice from different inbred lines homozygous forthe same gene knockout vary in the penetrance andexpressivity of the phenotype.e. Manipulations to create the knockout mouse, suchas the presence of a drug resistance gene that allowsthe selection of cells containing the knockout (seeFig. 18.9),…
Original DNA Sequence: TACAC CTTGG CGACGACT... MRNA Sequence: Amino Acid Sequence: Mutated DNA Sequence #5 TACACCTT G G GACGACT... (Highlight the change) What's the mRNA sequence? What will be the amino acid sequence? Will there likely be effects? What type of mutation is this? 1. Which type of mutation is responsible for new variations of a trait? 2. Which type of mutation does not result in an abnormal amino acid sequence? 3. Which type of mutation stops the translation of an mRNA molecule? NO
Which goals of the Human Genome Project do you think are themost important? Why? Discuss the types of ethical problems thatmight arise as a result of identifying all of our genes.
The ability to make modifications in the genomeprovides unlimited possibilities. With this, some groups raise publicconcerns about the possible negative effects of the widespread use andmanufacture of GM products. This makes genetic engineering a verycontroversial topic regarding its ethics. Write a 10 sentences reflection onthe pros and cons of genetic engineering, on a separate sheet of paper.
Answer the following MCQs: 1:This database is most likely to have data about gene expression. GenBank BLAST dbEST RefSeq PDB 2: Dot matris noise reduction: window size is 7 by 7 and mismatch is 2. What is the minimal number of matches in this window that allows us to place the dot? 2 3 1 5 4 3: Find the optimal global alignment of two DNA sequences _ACAAC and AC. Match = 2, mismatch =0, gap opening =-3, gap extention=-1. What is the total score of alignment? 2 -1 0 -3 1
4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3'...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5’ promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above). ii. Mutant B has a 2 G/C pairs inserted between position 19 and 20 (position denoted by the ^ in the sequence above).
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4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'...TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3' 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' * promoter
Silent mutations that occur in DNA are quite common in living cells and usually involve no effects on phenotype. Q) Provide one example of a clinical implication of a “silent mutation” that proven to have an effect onthe phenotype and provide a brief description of its molecular characteristics?
Give a schematic diagram of how we can Treatment Down's syndrome by using gene therapy? Please answer at your own words,please..
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