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 14P
| a. | Which genome manipulation technique would you use to create a mouse model for the human disease Leber congenital amaurosis (LCA), described at the very beginning of the chapter? Explain. |
| b. | Which procedure would you use to generate a mouse model for fragile X syndrome, a trinucleotide repeat disease caused by a mutant allele of the FMR-1 gene? (Review the Fast Forward Box in Chapter 7 entitled Trinucleotide Repeat Diseases: Huntington Disease and Fragile X Syndrome.) Explain. |
| c. | Which procedure would you use to create a mouse model for Huntington disease? |
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Cap, EA1, and Sap are all genes/proteins of interest in this study. For each gene, what gene product is encoded and where is the gene (the literal DNA sequence) located physically in the cell?
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC106848/
When the S.cerevisiae genome was sequenced and surveyed for possible genes, only about 40% of those genes had been previously identified in forward genetic screens. This left about 60% of predcited genes with no known function, leading some to dub the genes fun (function unknown) genes.
a)As an approach to understanding the function of a certain fun gene, you wish to create a loss of function allele. How would you do this?
b)You wish to know the physical location of the encoded protein product. How would you obtain such information?
this is what i have said about this image so far, what else can be said aswell including the raw count column.
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Interpreting the results of an RNA-Seq analysis is pivotal in understanding the underlying genetic mechanisms of diseases such as breast cancer. In this analysis, Figure 1 provides comprehensive data on differentially expressed genes associated with breast cancer. By delving into the provided information, we can gain valuable insights into the molecular landscape of this disease. First focus is on the gene with the highest fold change, EYA4, situated on chromosome 6. With a staggering fold change of 3604.4176, EYA4 exhibits an unprecedented level of overexpression in cancerous cells compared to normal cells. This profound alteration suggests a pivotal role for EYA4 in breast cancer pathogenesis. The log2 fold change of 11.81555 further emphasizes the magnitude of this difference in gene expression. Statistical significance is evident, with an exceptionally low p-value of…
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
- Which of the following conditions is most likely to be successfully treated by gene therapy using a viral vector to deliver a wild-type copy of one gene that is present in mutant form in a person with the condition? Assume that the viral vector used has the ability to home to relevant target tissues. Also assume that the patient can be treated at a young enough age to avoid irreversible phenotypic impacts of the mutation described. Timothy Syndrome, a multi-system disorder characterized by dysmorphic features and autistic behavioral traits, caused by overexpression of calcium channel gene Cerebral adrenoleukodystrophy (ALD), a neurological disorder caused by a frameshift mutation knocking out the function of the ABCD1 gene encoding a lipid transporter Osteogenesis imperfecta caused by a dominant negative mutation in the collagen A1 gene Myopia (shortsightedness), a vision impairment with heritability estimates in the range of 0.6-0.8, where risk is impacted by at least 200 genesarrow_forwarda. What is(are) the difference(s) between orthologs and paralogs? b. What are the main sources of variation? to search LGarrow_forwardExplain how site directed mutagenesis can be accomplished using M13 bacteriophage. Using this method often results in only 5% of plaques with mutant gene. Explain how the procedure has been modified to enrich for the number of plaques with the mutant gene.arrow_forward
- DNA hypermethylation (an excess of methylation) is associated with many neurological disorders, including a potential role in Alzheimer's disease. a. When comparing individuals with and without Alzheimer's, which of the following 'omics techniques (exome sequencing, whole genome sequencing, transcriptomics, or proteomics) would you expect to be the most informative if your goal is to locate potentially causative methylation differences? Briefly justify your answer. b. The pdCas9-Tet1-CD enzyme (Xu et al Cell Discov. 2016) fuses an enzyme that can carry out cytosine demethylation to a mutant version of the CRISPR/Cas9 enzyme that localizes to DNA using a guide RNA in exactly the same manner as we discussed in class for standard Cas9, except that this version does not cut the genome. This demethylase enzyme can then act to remove DNA methylation proximal to where it is stably bound. Imagine that you have identified a gene that is hypermethylated specifically in patients with Alzheimer's…arrow_forwardThe ability to selectively modify the genome in the mouse has revolutionized mouse genetics. Outline the procedure for generating a knockout mouse at a specific genetic locus. How can the loxP-Cre system be used to conditionally knock out a gene? What is an important medical application of knockout mice?arrow_forwardI get everything else in this problem other than the third option: Introduce the mutant human HD allele as a transgene into the mouse genome with transgene integration anywhere in the mouse genome. Why is the first question (left) okay with introducing mutant human HD allele and the second question (right) is not? I heard that introducing allele without using CRISPR-Cas9 is very rare and difficult. If so, how does it work in the first problem (Hungtinton's chorea)?arrow_forward
- Mutations in the HPRT1 gene in humans result in atleast two clinical syndromes. Consult OMIM (www.omim.org) by querying HPRT1; you will only needto look briefly at the top three hits (files #300322,300323, and 308000).a. What is the full name of the HPRT1 enzyme?b. On which chromosome is the HPRT1 gene located?c. Mutations in HPRT1 are associated with two different syndromes. What are these syndromes? Foreach, answer the following questions: (i) What arethe symptoms associated with the syndrome? (ii) Isthe mutant allele that causes the syndrome dominant, recessive, codominant, or incompletely dominant with respect to the normal allele, or do specialconditions apply? (iii) Is the syndrome associatedwith a loss-of-function or a gain-of-function disease allele? (iv) Does the syndrome display allelicheterogeneity? (v) Does the syndrome display locus heterogeneity? (Note: You do not need to understand everything in the OMIM entries to answerthese questions.)arrow_forwardThe accompanying photo shows a sequencing gel from the original study that first sequenced the cystic fibrosis gene (J. R. Riordan et al. 1989. Science 245:1066–1073). From the photo, determine the sequence of the normal copy of the gene and the sequence of the mutated copy of the gene. Identify the location of the mutation that causes cystic fibrosis. (Hint: The CF mutation is a 3-bp deletion.)arrow_forwardSTR markers: are point mutations detectable by DNA sequencing are variations in the number of repeats of very short DNA motifs (2-10 nucleotides) □have high polymorphism are mutations leading to proteins or blood groups that can be differentiated by antigenic testing from a blood sample ☐have low polymorphism no correct answer are changes of a few nucleotides leading to the absence or presence of a site recognized by a restriction enzyme are variations in the number of repeats of medium-sized DNA motifs (10-100 nucleotides) can be located in coding sequences are located exclusively on autosomesarrow_forward
- During 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_forwardNot all inherited traits are determined by nuclear genes (i.e., genes located in the cell nucleus) that are expressed during the life of an individual. In particular, maternal effect genes and mitochondrial DNA are notable exceptions. With these ideas in mind, let’s consider the cloning of a sheep (e.g., Dolly). A. With regard to maternal effect genes, is the phenotype of such a cloned animal determined by the animal that donated the enucleatedegg or by the animal that donated the somatic cell nucleus? Explain.arrow_forwardDifferent mutations in the WDR62 gene that inactivate gene function were found in the genomes of many different people with microcephaly. This information provided strong support for the idea that the WDR62 gene mutation causes microcephaly. A.The human genome sequence identified WDR62 as one of the approximately 27, 000 genes in the human genome. What information about the function of WDR62 do you think was learned originally from the DNA sequence of the normal human genome?arrow_forward
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