Principles of Biology
2nd Edition
ISBN: 9781259875120
Author: Robert Brooker, Eric P. Widmaier Dr., Linda Graham Dr. Ph.D., Peter Stiling Dr. Ph.D.
Publisher: McGraw-Hill Education
expand_more
expand_more
format_list_bulleted
Videos
Question
Chapter 16, Problem 7TY
Summary Introduction
Introduction:
Epigenetics lead to changes in the gene expression, which can be passed from cell to cell. The epigenetic modifications are reversible but do not involve in the change of DNA sequence. Some of the epigenetic changes may pass from parents to offspring, in epigenetic inheritance.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solution
Students have asked these similar questions
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.
Which of the following is true of tumor suppressor genes?
Group of answer choices
a) If this gene is overactive, it becomes an oncogene
b) If one of the alleles is mutated, there is usually little effect. Two inactivating mutations are usually required for loss of function (recessive mutation).
c) If one copy is lost, the gene no longer functions (dominant mutation)
d) Tumor suppressors genes usually cause mitosis or cell growth
e) Tumor suppressor genes decrease apoptosis
"In the cellular regulatory pathways that control cell growth and proliferation, the products of oncogenes are stimulatory components and the products of tumor suppressor genes are inhibitory components" is true or false.
Chapter 16 Solutions
Principles of Biology
Ch. 16.1 - Which of the following is an epigenetic change...Ch. 16.2 - If you crossed an Igf 2 Igf 2- male mouse to an...Ch. 16.2 - Prob. 1TYKCh. 16.2 - Prob. 2TYKCh. 16.3 - Prob. 1CCCh. 16.3 - Prob. 1TYKCh. 16.3 - Which of the following statements regarding...Ch. 16.4 - Prob. 1TYKCh. 16.4 - Prob. 2TYKCh. 16.5 - Prob. 1BC
Ch. 16.5 - Prob. 1CCCh. 16.5 - Prob. 1TYKCh. 16.5 - Prob. 2TYKCh. 16.6 - Prob. 1CCCh. 16.6 - Prob. 1BCCh. 16.6 - Prob. 1TYKCh. 16.6 - Genes that are linked do not conform to Mendels...Ch. 16 - Which of the following is an example of an...Ch. 16 - In mice, the allele of the Igf2 gene that is...Ch. 16 - Prob. 3TYCh. 16 - The marking process for genomic imprinting...Ch. 16 - According to Mary Lyons hypothesis, the patchwork...Ch. 16 - Prob. 6TYCh. 16 - Prob. 7TYCh. 16 - Prob. 8TYCh. 16 - Prob. 9TYCh. 16 - Prob. 10TYCh. 16 - Prob. 1CCQCh. 16 - Prob. 2CCQCh. 16 - Prob. 3CCQCh. 16 - Prob. 1CBQCh. 16 - Prob. 2CBQ
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
- Which of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growth-inhibiting factors to block cell division (c) more than 120 cancer-driving genes have been discovered (d) oncogenes were first discovered in mouse models for cancer (e) the development of cancer is usually a multistep process involving both oncogenes and mutated tumor suppressor genesarrow_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_forwardBRCA1 is a gene that codes for a tumor suppressor protein. If a person inherits a mutation in BRCA1, it greatly increases his or her risk of developing breast cancer. Are the cancer-causing mutations in the BRCA1 gene more likely to: A) not affect expression of the gene B) increase expression of the gene C) decrease expression of the genearrow_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_forwardCompare and contrast oncogenes and tumor suppressors. Contrast oncogenes and proto-oncogenes. Describe the types of mutations that convert proto-oncogenes into oncogenes. Summarize some functions of common oncogenes in cell survival and uncontrolled growth. Contrast tumor suppressors to oncogenes. Describe the types of mutations in tumor suppressors that are found in common cancers. Summarize the functions of common tumor suppressors in cell survival and cell growth.arrow_forwardA microarray is a technique used to develop a profile of the messenger RNA being transcribed by cells at a particular point in the life cycle of the cell. This allows the researcher to detect the expression of particular genes at a particular time. Microarrays have proven very useful in the detection of genes involved in certain types of cancer. If the product of a particular gene functions as a tumor suppressor, which piece of evidence do you think would be the most useful in the diagnosis of a cancer due to a nonsense mutation in this tumor-suppressor gene? (Hint: Don't worry about what a microarray is. Think about what you know about mitosis, cancer, and types of mutation.) O The tissue sample responds to treatment with a mitosis-promoting compound. O The tissue sample shows a high level of gene expression relative to a control (noncancerous) sample. O The mRNAs for the targeted tumor suppressor sequence are not being produced. O The mRNAs for cyclins and kinases show unusually high…arrow_forward
- Metastasis 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_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). Armed with your knowledge about the different mechanisms which govern transcription and translation, 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_forwardWhy does a single mutation in a proto-oncogene, turning it into an oncogene potentially lead to a cancerous phenotype, while it takes two mutations in tumor suppressor genes to lead to a cancerous phenotype?arrow_forward
- Genetic tests that detect mutations in the BRCA1 and BRCA2 tumor-suppressor genes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?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 protein p53 is activated when the cell's DNA is damaged. p53 helps to arrest the cell cycle in G1, allowing time for the cell to repair its DNA before replicating. p53 does this job by stimulating the synthesis of a protein that inhibits the cyclin-dependent kinase. Mutations that inactivate p53 contribute to 50% of human cancers. Would you classify p53 as a tumor-suppressor gene or a proto-oncogene?arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
Biology (MindTap Course List)BiologyISBN:9781337392938Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. BergPublisher:Cengage Learning
Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning
Biology (MindTap Course List)
Biology
ISBN:9781337392938
Author:Eldra Solomon, Charles Martin, Diana W. Martin, Linda R. Berg
Publisher:Cengage Learning
Human Heredity: Principles and Issues (MindTap Co...
Biology
ISBN:9781305251052
Author:Michael Cummings
Publisher:Cengage Learning
What are Mutations and what are the different types of Mutations?; Author: Science ABC;https://www.youtube.com/watch?v=I16YlE8qTBU;License: Standard youtube license