Genetics: Analysis and Principles
6th Edition
ISBN: 9781259616020
Author: Robert J. Brooker Professor Dr.
Publisher: McGraw-Hill Education
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Chapter 16, Problem 1EQ
Summary Introduction
To review:
The procedure of conducting a cell-fusion experiment for determining the nature of epigenetic modification involved in gene C silencing.
Introduction:
Epigenetics involves the study of genetic modifications that do not take place in DNA (deoxyribonucleic acid) but majorly modify its expression by switching it on or off. These changes can be reversible or irreversible. Some modifications include DNA acetylation or methylation, covalent modification of histone and their localization, chromatin remodeling, and activation of feedback loops, which is achieved using transcription factors and/ or non-coding RNAs (ribonucleic acid).
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A gene, which we will call gene C, can be epigenetically modified in such a way that its expression in some cells is permanently silenced. Describe how you could conduct cell-fusion experiments to determine if a cis- or a trans-epigenetic mechanism is responsible for maintaining the silencing of gene C.
What is the key difference between cis- and trans-epigenetic mechanisms for maintaining an epigenetic modification? We considered genomic imprinting of the Igf2 gene, in whichoffspring express the copy of the gene they inherit from their father,but not the copy they inherit from their mother. Is this a cisora trans-epigenetic mechanism?
In a qPCR experiment, you find that the mRNA for the gene CDK1 goes down (decreased expression) when you treat your cells with doxorubicin. You wonder whether this is due to epigenetic changes on the gene for CDK1. Name two methods that you might use to check whether there are changes in epigenetic modifications (e.g. DNA methylation or histone tail modifications) on the CDK1 DNA.
Chapter 16 Solutions
Genetics: Analysis and Principles
Ch. 16.1 - Which of the following are examples of molecular...Ch. 16.1 - 2. An epigenetic modification to a specific gene...Ch. 16.1 - Prob. 3COMQCh. 16.1 - Epigenetic changes may a. be programmed during...Ch. 16.2 - 1. For the Igf2 gene, where do de novo methylation...Ch. 16.2 - 2. For XCI to occur, where are the Xist and Tsix...Ch. 16.2 - 3. Which of the following possibilities could...Ch. 16.3 - 1. Which of the following statements about...Ch. 16.3 - The effects of paramutation may vary with regard...Ch. 16.4 - 1. When mice carrying theallele exhibit a darker...
Ch. 16.4 - 2. If the VIN3 gene had a loss-of-function...Ch. 16.5 - Prob. 1COMQCh. 16.5 - Prob. 2COMQCh. 16 - Prob. 1CONQCh. 16 - List and briefly describe five types of molecular...Ch. 16 - Prob. 3CONQCh. 16 - What is the key difference between cis and...Ch. 16 - Prob. 5CONQCh. 16 - Prob. 6CONQCh. 16 - 7. Outline the molecular steps in the process of...Ch. 16 - Prob. 8CONQCh. 16 - 9. In general, explain how epigenetic...Ch. 16 - 10. What are the contrasting roles of trithorax...Ch. 16 - Describe the molecular steps by which polycomb...Ch. 16 - Prob. 12CONQCh. 16 - Using coat color in mice and the development of...Ch. 16 - How can environmental agents that do not cause...Ch. 16 - Prob. 15CONQCh. 16 - Prob. 16CONQCh. 16 - Explain how the VIN3/PRC2 complex specifically...Ch. 16 - Prob. 1EQCh. 16 - In the experiments described in Figure 16.8,...Ch. 16 - Prob. 3EQCh. 16 - A research study indicated that an agent in...Ch. 16 - Lets suppose you were interested in developing...Ch. 16 - Prob. 6EQCh. 16 - Prob. 7EQCh. 16 - 2. Discuss the similarities and differences of...
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- Let’s suppose you were interested in developing drugs to preventepigenetic changes that may contribute to cancer. What cellularproteins would be the target of your drugs? What possible sideeffects might your drugs cause?arrow_forwardAlthough each cell in your body contains the same set of genes, the genes that are “turned on” differ depending on the type of cell. What signals different genes to be “turned on” or transcribed in different cells? What types of behaviours or environmental circumstances can lead to changes in an individual’s epigenome? Explain. 3. Explain how changes in your epigenome can alter the DNA of your future children before they are even born. 4.) Explain TWO implications of these findings for society. (Hint: think big! Implications for how disease is transmitted, intergenerational trauma, the cycle of poverty, etc.)arrow_forward"Tobacco smoking triggers a large number of somaticmutations and epigenetic changes". Define about this ?arrow_forward
- https://ny.pbslearningmedia.org/resource/biot09.sci.life.gen.epigenetics/epigenetics/ Explain DNA methylation. How does this process influence cellular function?arrow_forwardA geneticist uses a generic engineering approach to mutate the TATA-building protein (TBP) of a murine cell line that ordinarily produces high amounts of the LNS protein. The mutation prevents the binging of the TBP to the TATA box. What would be the effect on the cell line that possesses the mutation, especially LNS protein levels?arrow_forwardList and briefly describe five types of molecular mechanisms thatmay underlie epigenetic gene regulation.arrow_forward
- The rb gene encodes a protein that inhibits E2F, a transcriptionfactor that activates several genes involved in cell division.Mutations in rb are associated with certain forms of cancer,such as retinoblastoma. Under each of the following conditions,would you expect the cancer to occur?A. One copy of rb is defective; both copies of E2F are functional.B. Both copies of rb are defective; both copies of E2F arefunctional.C. Both copies of rb are defective; one copy of E2F is defective.D. Both copies of rb and E2F are defective.arrow_forwardAssume that there is a double stranded break on DNA double helix of an eukaryotic cell due to X-ray radiation and it is not repaired. In addition, the cell’s Apaf-1 protein is not expressed due to a null mutation in the Apaf-1 gene. Please discuss the effect of not having Apaf-1 expression in the cell with non-repaired double stranded break.arrow_forwardYou are analyzing the activity of the protein p53 in two different cell types. You notice that p53 has the same primary structure in both cells, but has a different function in each cell. What could be the reason for the functional difference in this case? A. p53 mRNA has been spliced differently in each cell type. B. p53 is phosphorylated on some amino acid residues in its transactivation domain in one cell type but not in the other cell type. C. The tetramerization domain of p53 is acetylated at the same amino acid residues in both cell types. D. All of the above E. B and C onlyarrow_forward
- Describe the 4 types of suppressor high copy suppression, bypass suppression, nonsense suppression, protein interaction . in your Own words. Often geneticists look for suppressors to find interactive proteins. Which of the type(s) of suppressors you put for part a will help to identify interacting proteins, and which type(s) will not? What are two (or one, if we don’t get a chance to talk about two of them in class) other techniques (not necessarily “genetic” techniques, but at least, lab techniques) that help to identify identifying proteins?arrow_forwardSeveral research studies are under way that involve the use of genetherapies to inhibit the growth of cancer cells. Oncogenes are mutant genes that are overexpressed and cause cancer. New gene therapies are aimed at silencing oncogenes by producing antisense RNA that recognizes the mRNAtranscribed from oncogenes. Based on your understanding of antisense RNA , explain how this strategy would prevent the growth of cancer cells.arrow_forwardWhich mechanisms for regulating gene expression may be applied for the treatment of such diseases? Propose a method of treatment. Explain how it might work. Reference: https://link.springer.com/article/10.1186/ar3317arrow_forward
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