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 4EQ
A research study indicated that an agent in cigarette smoke caused the silencing of a tumor-suppressor gene called p53. However, using sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.
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A research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.
Cellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase
protein, called Mdm2.
Over expression of Mdm2 destabilizes p53.
Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53.
Loss of p19ARF function converts normal cells into cancer cells
With the above information, which of the following statements are true?
Mdm2 is a tumor suppressor gene but p19ARF is an oncogene
Both Mdm2 & P19ARF are oncogenes
Both Mdm2 & P19ARF are tumor suppressor genes
O Mdm2 is an oncogene but p19ARF is a tumor suppressor gene
Describe error prone polymerases and the process of translesion synthesis (TLS). In regards to tumor biology, what is the mutator phenotype hypothesis? What are some ways in which error-prone polymerases could be targeted for potential anti-cancer treatments?
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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- D) The level of carbon dioxide increases with the level of available oxygen. 60) The TPS3 gene provides instructions for making a protein called tumor protein p53. Known as the guardlan of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing t0o fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will not…arrow_forwardD) The level of carbon dioxide increases with the level of available oxygen. 60) The TP53 gene provides instructions for making a protein called tumor protein p53. Known as the guardian of the genome, this protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing too fast or in an uncontrolled way. The p53 protein is located in the nucleus of cells throughout the body, where it attaches directly to DNA and plays a critical role in determining whether the DNA will be repaired or the damaged cell will self- destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. eg Suppose chromosomes in a skin cell are damaged by ultraviolet radiation. If the damaged genes do not affect p53, which choice correctly predict if the cell will become cancerous and why? No, the cell will…arrow_forwardResearchers have identified some tumors that have no recurrent mutations or deletions in known oncogenes or tumor-suppressor genes and no detectable epigenetic alterations. However, these tumors often have large chromosomal deletions. What are some possible explanations that could account for the genetic causes behind these tumors?arrow_forward
- The p53 gene was discovered in 1979, but it was not clear whether the gene functioned as an oncogene or a tumor-suppressor gene. Several years later, researchers showed that both p53 alleles are inactivated in some mouse cancers. This evidence suggests A. the p53 gene is an oncogene because inactivated alleles would produce mutated signal transduction proteins that would result in stimulating cell division. B. the p53 gene is an oncogene because the cell would overproduce transcription factors to compensate for the inactive alleles, resulting in increased cell division. C. the p53 gene is a tumor-suppressor gene because inactivated alleles indicate a loss of protein function which allowed the cancer to develop D. the p53 gene is a tumor-suppressor gene because the cell would produce too few transcription factors for gene activation, resulting in decreased cell division.arrow_forwardThe p53 gene is a tumor-suppressor gene while Ras is a proto-oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.arrow_forwardLi- Fraumeni Syndrome (LFS) is a rare hereditary cancer disease due to a mutation in the TP53 gene. Propose a treatment strategy for LFS.arrow_forward
- Tumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)arrow_forwardCancer is caused by many different types of gene mutations. Some mutations are in proto-oncogenes, which lead to overexpression of the genes, and other mutations are in tumor suppressor genes, which lead to under expression or no expression in these genes. Which kinds of gene mutations would RNA interference (RNAi) be better at treating? Explain.arrow_forwardRetinoblastoma is an extremely rare cancer of the retina in the eye. The disease mainly affects children up to the age of 5 years because it can only occur while the nerve precursor cells are still dividing. In its nonhereditary form, a tumor usually occurs in only one eye; in its hereditary form, multiple tumors develop in both eyes.To explore the basis for these differences, a cDNA clone of the Rb gene was used to probe the structure of the gene in cells from normal individuals and from individuals with nonhereditary or hereditary retinoblastoma. As shown in the figure Part A, normal individuals have four restriction fragments (A, B, C, and D) that hybridize to the Rb cDNA probe, indicating that each restriction fragment encodes at least one Rb exon. Samples from fibroblasts and tumor cells of affected persons show some differences in the patterns of hybridization, with some bands missing entirely and some bands present at half intensity. The order of the restriction fragments in the…arrow_forward
- The deregulation of several signal transduction pathways is integral to the onset of cancer. These pathways involve both tumor promoters (the "gas pedals") and tumor suppressors (the "brake pedals"). Which would be a more effective treatment for cancer: A small molecule inhibitor that targets a tumor suppressor or one that targets a tumor promoter? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.) Edit View. Insert Format Tools Table 12pt v Paragraph BI UAV 2VT² V| :arrow_forwardCancer often results from a multistage process involving an initiating event (mediated by a viral infection or a carcinogenic chemical), followed by exposure to tumor promoters. Tumor promoters, a group of molecules that stimulate cell proliferation, cannot induce tumor formation by themselves. The phorbol esters, found in croton oil (obtained from the seeds of the croton plant, Croton tiglium), are potent tumor promoters. (Other examples of tumor promoters include asbestos and several components of tobacco smoke.) In one of the tumor-promoting actions of the phorbol esters, these molecules mimic the actions of DAG. In contrast to DAG, the phorbol esters are not easily disposed of. Explain the possible biochemical consequences of phorbol esters in an “initiated” cell. What enzyme is activated by both DAG and phorbol esters?arrow_forwardThe 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_forward
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