EBK GENETICS: FROM GENES TO GENOMES
6th Edition
ISBN: 9781260041255
Author: HARTWELL
Publisher: MCGRAW HILL BOOK COMPANY
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Chapter 20, Problem 16P
Why don’t all loss-of-function mutations that are recessive at the cellular level behave as dominants at the organismal level? Is this property restricted to tumor-suppressor gene mutations?
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Why don’t all loss-of-function mutations that are recessive at the cellular level behave as dominants at the organismal level? Is this property restricted to tumor-suppressor gene mutations?
Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.
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…
Chapter 20 Solutions
EBK GENETICS: FROM GENES TO GENOMES
Ch. 20 - For each of the terms in the left column, choose...Ch. 20 - Characterize the differences between tumor cells...Ch. 20 - Prob. 3PCh. 20 - Prob. 4PCh. 20 - A carcinogenic compound is placed on the skin of...Ch. 20 - You have decided to study genetic factors...Ch. 20 - B cells are specialized blood cells that secrete...Ch. 20 - Molecules outside and inside the cell regulate the...Ch. 20 - Put the following steps in the correct ordered...Ch. 20 - a. Would you expect a cell to continue or to stop...
Ch. 20 - Two different protein complexes called SCF and APC...Ch. 20 - One of the hallmarks of mitotic anaphase is the...Ch. 20 - Concerning the Tools of Genetics Box Analysis of...Ch. 20 - Are genome and karyotype instabilities...Ch. 20 - Prob. 15PCh. 20 - Why dont all loss-of-function mutations that are...Ch. 20 - Chromothripsis is a rare phenomenon, first...Ch. 20 - The chromosome 9/22 translocation associated with...Ch. 20 - A female patient 19 years old, whose symptoms are...Ch. 20 - Prob. 20PCh. 20 - A generic signaling cascade is shown in the...Ch. 20 - Neurofibromatosis type 1 NF1; also known as von...Ch. 20 - Families with germ-line BRCA1 or BRCA2...Ch. 20 - The text explained that retroviruses can cause...Ch. 20 - Hepatocellular carcinoma is the most frequent form...Ch. 20 - Suppose that instead of microarrays, you analyzed...Ch. 20 - Prob. 27PCh. 20 - Glioblastoma multiforme GBM is the most common and...Ch. 20 - a. The legend to Fig. 20.29 identifies which of...Ch. 20 - The website CBioPortal http://www.cbioportal.org...
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- Why are oncogenes usually dominant in their action, whereas tumor-suppressor genes are recessive?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_forwardDescribe how mutations in genome maintenance factors promote tumorigenesis. Why would inactivation of a mis- match repair gene cause colon cancer?arrow_forward
- 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 genearrow_forwardWhat are Ras protein and p53? How can mutations in the genes for these proteins contribute to cancer?arrow_forwardDefine tumor-suppressor genes. Why is a mutated single copy of a tumor-suppressor gene expected to behave as a recessive gene?arrow_forward
- Define tumor-suppressor genes. Why is a mutation in a single copy of a tumor-suppressor gene expected to behave as a recessive gene?arrow_forwardWhy don’t all loss-of-function mutations that are recessive at the cellular level behave as dominants at theorganismal level? Is this property restricted to tumorsuppressor gene mutations?arrow_forwardWhat would be the effect of a mutation that inactivates the p14ARF tumor suppressor upon p53 functions?arrow_forward
- Cancer 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_forwardThe Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!arrow_forwardMetastasis occurs when cells from a primary tumor invade and colonize other tissues. Metastasis is a complex, multistep process. Tumor cells must lose adhesion with other tumor cells, invade local tissues and vessels, move through the circulation, leave the vessels, and finally, establish new colonies at distant sites. Tumor cells gain the ability to cross epithelial layers and migrate through tissues by mutations, although the nature of the mutations that drive metastasis is poorly understood. Mutations that block expression of the E-cadherin gene are thought to be an important step in metastasis. The absence of E-cadherin expression could affect metastasis by blocking cell adhesion directly, by releasing signaling proteins bound to the cytoplasmic domain of E-cadherin, or by both mechanisms. To better understand how loss of E-cadherin contributes to metastasis, scientists created two cell lines that differed in their expression of E-cadherin. One cell line was blocked for expression…arrow_forward
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