Campbell Biology (11th Edition)
11th Edition
ISBN: 9780134093413
Author: Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, Jane B. Reece
Publisher: PEARSON
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Chapter 15.4, Problem 3CC
Summary Introduction
To determine: The activation of the gene on Philadelphia chromosome that codes for intracellular tyrosine kinase, contributing to the development of cancer.
Concept introduction:
Tyrosine kinase belongs to the group of protein kinases. It catalyzes the addition of a phosphate group from the ATP molecule generated, to a protein molecule. This addition aids in transferring a signal that induces the cell to divide.
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List and describe 4 of the main regulators of the cell cycle. Then describe the involvement of a CDK substrate at each stage of the cell cycle: G1, S, G2, M.
2. DESCRIBE (do not just list) three mechanisms that keep the cell cycle moving in only one direction. Then describe how these mechanisms play a role at one specific stage of the cell cycle.
3. What are the three main classes of genes implicated in cancer? Describe each one and give an example of each one.
4. DESCRIBE (do not just list) 4 developmental strategies that cause different cells and tissues to acquire different identities during embryogenesis. Then explain how iPS cells are an exception to the overall trend of cells decreasing in pluripotency as they develop.
5. Describe three unique cell biological features of sperm cells and three unique cell biological features of egg cells. By "unique", I mean a feature that is not common in most cells.
6. You have just identified a mouse gene that is homologous to other vertebrate…
Modify 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.
. MAKE CONNECTIONS The p53 protein can activategenes involved in apoptosis. Review Concept 11.5, anddiscuss how mutations in genes coding for proteins thatfunction in apoptosis could contribute to cancer.
Chapter 15 Solutions
Campbell Biology (11th Edition)
Ch. 15.1 - Which one of Mendel's laws describes the...Ch. 15.1 - MAKE CONNECTIONS Review the description of...Ch. 15.1 - WHAT IF? Propose a possible reason that the first...Ch. 15.2 - A white-eyed female Drosophila is mated with a...Ch. 15.2 - Neither Tim nor Rhoda has Duchenne muscular...Ch. 15.2 - MAKE CONNECTIONS Consider what you learned about...Ch. 15.3 - When two genes are located on the same chromosome,...Ch. 15.3 - VISUAL SKILLS For each type of offspring of the...Ch. 15.3 - Prob. 3CCCh. 15.4 - Prob. 1CC
Ch. 15.4 - Prob. 2CCCh. 15.4 - Prob. 3CCCh. 15.5 - Gene dosagethe number of copies of a gene that are...Ch. 15.5 - Reciprocal crosses between two primrose varieties,...Ch. 15.5 - WHAT IF? Mitochondrial genes are critical to the...Ch. 15 - What characteristic of the sex chromosomes allowed...Ch. 15 - Why are males affected by X-Iinked disorders much...Ch. 15 - Why are specific alleles of two distant genes more...Ch. 15 - Prob. 15.4CRCh. 15 - Explain how genomic imprinting and inheritance of...Ch. 15 - A man with hemophilia (a recessive, sex-linked...Ch. 15 - Pseudohypertrophic muscular dystrophy is an...Ch. 15 - A wild-type fruit fly (heterozygous for gray body...Ch. 15 - A planet is inhabited by creatures that reproduce...Ch. 15 - Using the information from problem 4, scientists...Ch. 15 - A wild-type fruit fly (heterozygous for gray body...Ch. 15 - Assume that genes, A and B are on the same...Ch. 15 - Two genes of a flower, one Controlling blue (B)...Ch. 15 - You design Drosophila crosses to provide...Ch. 15 - Banana plants, which are triploid, are seedless...Ch. 15 - EVOLUTION CONNECTION Crossing over is thought to...Ch. 15 - SCIENTIFIC INQUIRY DRAW IT Assume you are mapping...Ch. 15 - WRITE ABOUT A THEME: INFORMATION The continuity of...Ch. 15 - SYNTHESIZE YOUR KNOWLEDGE Butter flies have an X-Y...
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- Despite being small animals, naked mole rats are almost entirely resistant to cancer. Watch the following brief video on one potential mechanism for the prevention of cancer in naked mole rats. https://youtu.be/bhNBeuhxkF0?si=38aelHLW1N6vN8-b Based on what you know about mitosis and cancer cells, why would a mechanism that prevents cell crowding reduce the likelihood of cancer developing?arrow_forwardExplain the concept of loss of heterozygosity (LOH). Why do most cancer cells exhibit LOH of one or more genes? How does failure of the spindle assembly checkpoint lead to loss of heterozygosity?arrow_forwardDescribe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.arrow_forward
- Describe three changes in cell cycle control and regulatory proteins that lead to cancer.arrow_forwardA. Name the two proteins that induce a negative feedback in this pathway and explain why both feedback mechanisms exist? B. Discuss how a mutation resulting in an aberrant protein could cause changes in the cell cycle leading to uncontrolled cell division. Explain what the effect of the mutation would be on the protein’s function and what the effect will be on downstream proteins leading to enhanced cell cycle progressionarrow_forwardDiscuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.arrow_forward
- Describe the effects of the mutation causing the p21 promoter to no longer bind p53 on cell signaling pathways and metabolism or cell cycle control.arrow_forwardQ. Cyclins and CDK(inase) complexes regulate the cell cycle. Which of the following statements is true? A. Cyclins activate CDKs which remove phosphates from other proteins. B. Cyclins activate CDKs which add phosphates to other proteins. C. CDKs activate cyclins which remove phosphates from other proteins. D. CDKs activate cyclins which add phosphates to other proteins.arrow_forwardWhen regulating the cell cycle of eukaryotic cells, a critical protein we discussed was cyclin. Cyclin is Select one: a. Always present in all stages of the cell cycle, but only active during the G1 - R transition b. Produced in response to signals for the cell to divide c. Produced only when retinoblastoma protein is inactivated d. Produced in response to the presence of cyclin-dependent kinasearrow_forward
- After DNA damage (e.g. caused by X-ray exposure) in eukaryotic cells, the cell cycle can be arrested by the stabilisation of the protein which drives the transcription of the gene, whose protein product interacts with the G1/S-Cdk and S-Cdk complexes. O PDGF, acetyltransferase O phenylalanine hydraxylase, PDGF O p53, acetyltransferase O p53, p21 O p21. p53arrow_forwardp53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?arrow_forwardDescribe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?arrow_forward
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