Genetics: Analysis and Principles
6th Edition
ISBN: 9781259616020
Author: Robert J. Brooker Professor Dr.
Publisher: McGraw-Hill Education
expand_more
expand_more
format_list_bulleted
Concept explainers
Videos
Textbook Question
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.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
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
Why is it important to model cancer through the generation of induced pluripotent stem cells ?
Explain in detail the main findings. Please sort as a list.
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...
Knowledge Booster
Learn more about
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
- 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_forwardDescribe 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?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
- D) 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_forwardp53 is a tumor suppressor gene in human cells. Transcription of this gene leads to the production of the p53 protein in cells which modulates many signal pathways that lead to anti-tumor effects. The strength of anti-tumor effects is directly porportional to the accumulation of the protein within the cells of the person. Suppose a pediatric patient was recently admitted for a rare lung cancer related to p53 deficiencies (although the p53 itself is not mutated). what are some potential reasons for the deficiency in p53 levels and how can you restore them if the reason you assumed for the deficiency is not directly reparable (i.e if you assume that protein degradation is too fast, you cannot directly repair protein degradation but you may want to increase transcription & translation rates to compensate)? Will your hypothesized repair(s) cause negative impacts to the cell? Why?arrow_forwardThe 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_forward
- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.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_forwardLoss of p53 function occurs in the majority of human tumors. Name two ways in which loss of p53 function contributes to a malignant phenotype. Explain how benzo(a) pyrene can cause loss of p53 function.arrow_forward
- Why is it important to model cancer through the generation of induced pluripotent stem cells ? Please list item by item. Explain in detail the main findings.arrow_forwardTumor-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_forwardTumor suppressor proteins can assist in slowing down the cell cycle under appropriate conditions. In humans, the TP53 gene encodes a tumor suppressor called p53. Most mutations in the TP53 gene result in a mutant form of p53 that can no longer function to slow down the cell cycle, which can lead to a cell becoming cancerous. However, some mutant forms of p53 actually possess the ability to increase a cell's resistance to anticancer treatments. Which of the following BEST describes the latter type of mutation? loss-of-function mutation gain-of-function mutation suppressor mutation reverse mutationarrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning
Human Heredity: Principles and Issues (MindTap Co...
Biology
ISBN:9781305251052
Author:Michael Cummings
Publisher:Cengage Learning
An Introduction to the Human Genome | HMX Genetics; Author: Harvard University;https://www.youtube.com/watch?v=jEJp7B6u_dY;License: Standard Youtube License