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 11P
The 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 a mutation in every gene in the mouse genome.
| a. | Do you think that it will be possible, for every gene, to generate a heterozygous knockout ES cell line? Explain. |
| b. | Do you think that for every heterozygous knockout ES 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 described in Problem 5. How could these researchers use ES cell technology to determine whether Fam is required for eye development in the mouse? Diagram a construct that the researchers could introduce into ES cells to explore this issue. |
| d. | Describe various outcomes that might be obtained from the experiment in part (c) and what you could conclude in each case. |
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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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- In the module, you have learned about P-element mediated transgenesis in Drosophila and the concept of using transgenes to rescue mutant phenotypes. In the figure below, you will see a wild type fly with its natural eye colour and three mutants with their eye colours changed to vermillion, white and rosy, respectively. A schematic of P-element mediated transgenesis (as shown in the lectures) is also included in the figure. Please inspect the schematic carefully and choose which of the following statements is true: I. Injection of the white experimental transgene into the vermillion mutant embryo will not change the vermillion mutant phenotype II. Injection of the white experimental transgene in the rosy mutant embryo will change rosy eye colour to red (wild type) III. Injection of the white experimental transgene in the white mutant embryo will not change the white mutant phenotype IV. Injection of the white experimental transgene in the rosy mutant…arrow_forwarda. Describe two ways you could potentially make atransgene that would inhibit the function of a specific gene in a transgenic organism. (Hint: For oneof these techniques, recall the discussion of RNAinterference in Chapter 17.)b. Discuss how you could use either of these methodsto construct a mouse model for a recessive humangenetic condition associated with a loss of function, such as cystic fibrosis.arrow_forwardYou identify a mouse mutant that has hemophilia and is unable to properly clot blood. Your assays reveal that a novel clotting factor is absent from the blood of the mutant mice. You sequence the genome of the mutant mouse and determine that clotting factor proteins normally associated with hemophilia are all wildtype (no mutations), but the coding sequence of the novel protein differs by one amino acid compared to wildtype. When you synthesize the mutant protein in vitro, it has normal blood clotting activity. Your controls using other mutant hemophilia clotting proteins fail to clot blood in this assay. What would you say the mutant protein results in hemophelia?arrow_forward
- Mice usually have wild-type agouti fur that appears grey, but a mouse geneticist has a pure-breeding white-furred strain that is homozygous for a recessive mutation. Molecular analysis shows that the mutation is a missense mutation in an exon common to three alternatively spliced forms of a gene expressed in hair follicles. Which of the following transgenic animals would be most useful to determine which spliced form (or forms) is sufficient to specify agouti fur?A. Construct a GFP reporter using the promoter for the identified gene. B. Express a wild-type version of a cDNA for each spliced form in the white mutant mouse to see which form(s) rescue the phenotype. C. Use CRISPR/Cas9 to make a large deletion of the entire coding region of the identified gene. D. Introduce the wild-type genomic allele into the mutant mouse to test for rescue of the mutant phenotypearrow_forwardWhich of the four constructs (Construct 1-4) could be made to make a knockout mouse? For each one not chosen explain why you did not that construct.arrow_forwardA. Do you have any mature transcripts that show alternative splicing? If so, give an example by naming two transcripts that differ in this way. If your gene does not have this difference, write "no". B. Do you have any transcripts that have an alternative transcription start sites? If so, give an example by naming two transcripts that differ in this way. If your gene does not have this difference, write "no". C. Do you have any transcripts that have an alternative termination sites? If so, give an example by naming two transcripts that differ in this way. If your gene does not have this difference, write "no".arrow_forward
- A graduate student studying yfgA expression in the liver and heart performs an RNA-seq experiment. She aligns her sequencing reads to the human genome as shown. a.) What splice variants are expressed in the liver? Draw the mRNA and label the exons.b.) Are they expressed at the same levels in the liver? Explain c.) What splice variants are expressed in the heart. Clearly explain all the data from the figure. d.) In which tissue is the gene more highly expressed? Explainarrow_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_forwarda. Why is it impossible to induce nonsense mutations(represented at the mRNA level by the triplets UAG,UAA, and UGA) by treating wild-type strains with mutagens that cause only A• G → T• C transitions in DNA?b. Hydroxylamine (HA) causes only G• C → A• T transitions in DNA. Will HA produce nonsense mutations inwild-type strains?c. Will HA treatment revert nonsense mutations?arrow_forward
- When disrupting a mouse gene by knockout, why is it desirable to breed mice until offspring homozygous (-/-) for the knockout target gene are obtained?arrow_forwardExplain one experimental strategy for determining the functional role of the mouse HoxD-3 gene.arrow_forwardUsing RNA-seq analysis of transcripts isolated from different organs in mice, you find that the GFAPgene is expressed only in the brain. You examine expression in glia and neurons (two different celltypes found in the brain) and determine that GFAP mRNA and protein is made only in glia. Thisgene has never been studied before, so you start by characterizing the cis-acting elements requiredfor brain-specific expression. a. You decide to fuse pieces of DNA found upstream regions of the coding region of GAP to areporter gene (lacZ) and monitor expression. Different fragments (shown as dark lines) werecloned next to the lac gene that lacked its own promoter. M and H are restriction enzymesites. From the data shown, determine which region contains the promoter and whichregion contains an enhancer . Explain.arrow_forward
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