Concepts of Genetics (12th Edition)
12th Edition
ISBN: 9780134604718
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino, Darrell Killian
Publisher: PEARSON
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Chapter 15, Problem 13PDQ
DNA damage brought on by a variety of natural and artificial agents elicits a wide variety of cellular responses involving numerous signaling pathways. In addition to the activation of DNA repair mechanisms, there can be activation of pathways leading to apoptosis (programmed cell death) and cell-cycle arrest. Why would apoptosis and cell-cycle arrest often be part of a cellular response to DNA damage?
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A cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation?
A) This cell would have a cancer phenotype
B) This cell would grow larger in size, but would never divide
C) This cell would likely undergo apoptosis
D) This cell would not duplicate its chromosomes
.
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…
During cell division cycle, cells need to monitor the process of DNA replication and segregation of
replicated DNA so that these processes are error-free. Some potential errors that could occur include
incomplete DNA replication, DNA damage in genome, and uneven separation of replicated genome.
These mechanisms that cells used to monitor these processes are referred as the "cell cycle checkpoint,
which can control specific Cdk activity to regulate the progression of cell cycle. For the following
checkpoint mechanisms, indicate which Cdk activity is attenuated? Also indicate one of the key proteins
or protein complexes involved in the following checkpoints.
a) DNA damage checkpoint during S-phase
b) Mitotic checkpoint during M-phase
Chapter 15 Solutions
Concepts of Genetics (12th Edition)
Ch. 15 - If a point mutation occurs within a human egg cell...Ch. 15 - One of the most famous cases of an X-linked...Ch. 15 - The cancer drug melphalan is an alkylating agent...Ch. 15 - Geneticists often use the alkylating agent...Ch. 15 - Six months pregnant, an expectant mother had a...Ch. 15 - Six months pregnant, an expectant mother had a...Ch. 15 - HOW DO WE KNOW? In this chapter, we focused on how...Ch. 15 - CONCEPT QUESTION Review the Chapter Concepts list...Ch. 15 - What is a spontaneous mutation, and why are...Ch. 15 - Prob. 4PDQ
Ch. 15 - Prob. 5PDQCh. 15 - Why is a random mutation more likely to be...Ch. 15 - Most mutations in a diploid organism are...Ch. 15 - What is the difference between a silent mutation...Ch. 15 - Describe a tautomeric shift and how it may lead to...Ch. 15 - Contrast and compare the mutagenic effects of...Ch. 15 - Why are frameshift mutations likely to be more...Ch. 15 - Why are X rays more potent mutagens than UV...Ch. 15 - DNA damage brought on by a variety of natural and...Ch. 15 - Contrast the various types of DNA repair...Ch. 15 - Mammography is an accurate screening technique for...Ch. 15 - A significant number of mutations in the HBB gene...Ch. 15 - Describe how the Ames test screens for potential...Ch. 15 - Prob. 18PDQCh. 15 - Compare DNA transposons and retrotransposons. What...Ch. 15 - Prob. 20PDQCh. 15 - In maize, a Ds or Ac transposon can alter the...Ch. 15 - Prob. 22PDQCh. 15 - In a bacterial culture in which all cells are...Ch. 15 - Presented here are hypothetical findings from...Ch. 15 - Prob. 25ESPCh. 15 - Prob. 26ESPCh. 15 - What evidence indicates that mutations in human...Ch. 15 - Among Betazoids in the world of Star Trek, the...Ch. 15 - Skin cancer carries a lifetime risk nearly equal...Ch. 15 - It has been noted that most transposons in humans...Ch. 15 - Mutations in the IL2RG gene cause approximately 30...
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- Overexpression of the Myc protein is a common feature of many types of cancer cells, contributing to their excessive cell growth and proliferation. By contrast, when Myc is overexpressed in most normal cells, the result is not excessive proliferation, but cell-cycle arrest or apoptosis.Which one of the following statements provides the most likely explanation for why overexpression of Myc can have such different outcomes in normal cells and in cancer cells? A. Normal cells contain checks and balances that prevent Myc-induced proliferation. B. In normal cells, Myc protein acts as a mediator in cell-cycle arrest and apoptosis. C. The target protein for Myc-induced proliferation is missing from most normal cells. D. In normal cells, when Myc is overexpressed, the excess Myc protein precipitates.arrow_forwardWhich is true for cancer cells: 1) Cell death occurs after a determined number of cell divisions 2) Contact with other cells reduces chance of cell division 3) Cell division occurs in the presence of stop signals.arrow_forwardIdentify and list the functions of the three general classes of proteins that control cell death.arrow_forward
- You are studying the function of Bax as a positive regulator of apoptosis. You've engineered a version of the Bax protein that is functional, but is mislocalized to the plasma membrane rather than the mitochondria. You expect that this will block the intrinsic pathway of apoptosis. When you activate the intrinsic pathway of apoptosis, you are surprised to find that the cells still die. You then do a cell fractionation experiment and verify that Bax is. indeed being sent to the plasma membrane, rather than the mitochondria. In one sentence, what is the most likely hypothesis for what is happening?arrow_forwardD) 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_forwardCellular 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 genearrow_forward
- Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth. the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.arrow_forward(46) A mutated form of protein p5x is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bin d to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteinsarrow_forwardWhat is a possible outcome of the addition of a transcription factor such as Myod to the nucleus of a cell? Assume that there are no other factors to either activate or prevent the response of the cell. Group of answer choices A) Production of mRNA from genes that were previously not expresed B)adding methyl groups to DNA C)prevention of protein synthesis D)uncoiling of the chromatin to allow transcriptionarrow_forward
- Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.arrow_forwardModify the diagram above to illustrate specific protein(s) that would participate in regulating this pathway if DNA damage was detected in these cells. What effect would this have on the progression of the cell cycle? If there is more than one possible outcome be sure to outline each one.arrow_forward(46) A mutated form of protein pox is found in patients with squamous cell carcinoma. In vitro studies show that the normal p5x molecule binds to DNA, and neoplastic cells accumulate in the G0 phase of the cell cycle. In contrast, the mutated form of p5x does not bind to DNA. These finding are most characteristics of which of the following? (A) Growht factor receptors (B) GTP-binding protein (C) Nonreceptor tyrosine kinases (D) Oncogene proteins (E) Tumor suppressor gene proteinsarrow_forward
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