Genetics: From Genes to Genomes
6th Edition
ISBN: 9781259700903
Author: Leland Hartwell Dr., Michael L. Goldberg Professor Dr., Janice Fischer, Leroy Hood Dr.
Publisher: McGraw-Hill Education
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Chapter 18, Problem 19P
Mouse models for human genetic diseases are potentially powerful tools to help geneticists understand the cause of the aberrant
| a. | Mice have a shorter life span than humans. |
| b. | Mice homozygous for certain knockout mutations die in utero. |
| c. | Mouse genomes may have additional copies of the gene whose mutation causes the disease in humans. |
| d. | Mice from different inbred lines homozygous for the same gene knockout vary in the penetrance and expressivity of the phenotype. |
| e. | Manipulations to create the knockout mouse, such as the presence of a drug resistance gene that allows the selection of cells containing the knockout (see Fig. 18.9), can disrupt not only the targeted gene, but also the expression of other, nearby genes. |
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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.
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Chapter 18 Solutions
Genetics: From Genes to Genomes
Ch. 18 - Match each of the terms in the left column to the...Ch. 18 - Mice are usually gray, but a mouse geneticist has...Ch. 18 - Sometimes, genes transferred into the mouse genome...Ch. 18 - In mice, a group of so-called Hox genes encode...Ch. 18 - The fly eyes shown in Fig. 18.7 are malformed...Ch. 18 - This problem concerns a technique called enhancer...Ch. 18 - Fish and other organisms that live in the Arctic...Ch. 18 - a. Describe two ways you could potentially make a...Ch. 18 - Figure 18.6 shows a picture of Glofish ,...Ch. 18 - Some people are concerned about the possible...
Ch. 18 - The goal of the Knockout Mouse Project is to...Ch. 18 - Prob. 12PCh. 18 - Prob. 13PCh. 18 - a. Which genome manipulation technique would you...Ch. 18 - a. Diagram a knockin construct that could have...Ch. 18 - Prob. 16PCh. 18 - Prob. 17PCh. 18 - The transcription factor Pax6 is required...Ch. 18 - Mouse models for human genetic diseases are...Ch. 18 - One way to determine where inside a cell a protein...Ch. 18 - In Problem 5 in Chapter 17, you saw that a SNP...Ch. 18 - Scientists now routinely use CRISPR/Cas9 to make...Ch. 18 - Geneticists are currently considering using...Ch. 18 - a. Figures 18.9 and 18.12 demonstrated methods to...Ch. 18 - Nonhomologous end-joining NHEJ of a double-strand...Ch. 18 - One problem that researchers sometimes encounter...Ch. 18 - Researchers at the University of California at San...Ch. 18 - Prob. 28PCh. 18 - F. Port and S. Bullock at the University of...Ch. 18 - On Fig 18.14, locate the PAM site and identify the...Ch. 18 - Prob. 31PCh. 18 - Prob. 32PCh. 18 - Recall that Leber congenital amaurosis LCA, a form...Ch. 18 - One potential strategy for gene therapy to correct...Ch. 18 - Recently, scientists have used a mouse model for...
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Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- i) Suppose we want to insert the GFP sequence after the promoter of a gene X to create a fusion protein. Please describe the strategy that you will follow to edit this gene with CRISPR-Cas9 technology, in order to visualize the expression of gene X in live cells. (ii) Please explain how a knockout mouse for a gene X can be produced with CRISPR-Cas9 technologyarrow_forwardThe goal of the Knockout Mouse Project is to generate a set of ES cell lines, each with a knockout mutation in a single gene, that collectively contains amutation in every gene in the mouse genome.a. Do you think that it will be possible, for everygene, to generate a heterozygous knockout ES cellline? Explain.b. Do you think that for every heterozygous knockoutES cell line, it will be possible to generate a heterozygous knockout mouse? Explain.c. In fact, investigators failed in their attempts to generate ES cell knockouts for the Fam gene describedin Problem 5. How could these researchers use EScell technology to determine whether Fam is required for eye development in the mouse? Diagrama construct that the researchers could introduceinto ES cells to explore this issue.d. Describe various outcomes that might be obtainedfrom the experiment in part (c) and what you couldconclude in each case.arrow_forwardTwo approaches for correcting single-gene defects are gene therapy such as is discussed in Section 3-5D and the CRISPR–Cas9 system. Explain why the CRISPR–Cas9 approach can potentially provide more complete restoration of normal tissue function than gene therapy.arrow_forward
- if you encounter an unknown disease in humans and would like to understand the genetic mechanism for this disease so that an effective and targetted treatment approach can be developed , what will be the best strategy or steps to accomplish the goal? NB :answer in at most 4 sentences.arrow_forwardNow that you understand how the CRISPR-Cas9 system works, think back to the experiments discussed in the introduction to this chapter, in which researchers used CRISPR-Cas9 genome editing to treat mice with Duchenne muscular dystrophy. Why did the researchers choose to cut out the entire exon 23 in the mice with the disorder? Why not replace the specific mutation using a donor piece of DNA and homologous recombination? Propose some possible explanations.arrow_forwardDuring construction of a knockout mouse, a targeting vector is introduced into mouse embryonic cells, where it integrates into the genome at a ["targeted site", "random location"] by ["homologous recombination", "nonhomologous end joining "] . Pick answers within quotation marks to fill in the blanks.arrow_forward
- In the bacteriophage T7 system used to express recombinant proteins, the gene of interest is fused to T7 promoter and T7 RNA polymerase is separately cloned into the same cell. What is the main reason this system uses T7 RNA polymerase instead of relying on the bacterial RNA polymerase? To restrict the expression of bacterial protein expression To enhance the amount of recombinant protein expression To enhance the expression of bacterial protein expression To restrict the amount of recombinant protein expression To enable the expression of T7 viral protein expressionarrow_forwardIf you wanted to make a mouse model for any of the following human genetic conditions (a–d), indicate which of thefollowing types of mice (i–vi) would be useful to your studies. If more than one answer applies, state which type ofmouse would most successfully mimic the human disease:(i) transgenic mouse overexpressing a normal mouse protein; (ii) transgenic mouse expressing normal amounts of amutant human protein; (iii) transgenic mouse expressing adominant negative form of a protein; (iv) a knockout mouse;(v) a conditional knockout mouse; and (vi) a knockin mousein which the normal allele is replaced with a mutant allelethat is at least partially functional. In all cases, the transgeneor the gene that is knocked out or knocked in is a form of thegene responsible for the disease in question.a. Marfan syndrome (a dominant disease caused byhaploinsufficiency for the FBN1 gene);b. A dominantly inherited autoinflammatory diseasecaused by a hypermorphic missense mutation in thegene PLCG2;c.…arrow_forwardThe 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-globinarrow_forward
- Describe the methodology that you would use to determine the association between specific sequence variations or epigenetic modifications and observed diseases in humans. Given your newfound knowledge of this association how would you then design a genetic test that could be used to identify individuals within a given population who have developed the disease or at risk of developing the disease. “The disease” here refers to any heritable genetic disease..arrow_forwardWhat is a simple way of making a knockout mouse in terms of DNA recombinant technology?arrow_forwardIn contrast with the genomic manipulations of animals and plants described in this chapter, human genetherapy is directed specifically at altering the genomes of somatic cells rather than germ-line cells.Why couldn’t or wouldn’t medical scientists try to alter the genome of human germ-line cells?arrow_forward
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Mitochondrial mutations; Author: Useful Genetics;https://www.youtube.com/watch?v=GvgXe-3RJeU;License: CC-BY