When a particular mutagen is identified by the Ames test and injected into mice (group A), it causes tumors, showing that the substance in carcinogenic. When cells from those tumors are injected into mice that were not exposed to the mutagen, the new mice get tumors (group B). However, when mice with tumors are mated to unexposed mice, no tumors are seen in the offsprings (group C). Explain why each of these mice get/do not get tumors and the nature of those tumors (environmental/inherited).
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![9. When a particular mutagen is identified by the Ames test and injected into mice (group A), it causes
tumors, showing that the substance in carcinogenic. When cells from those tumors are injected into mice
that were not exposed to the mutagen, the new mice get tumors (group B). However, when mice with
tumors are mated to unexposed mice, no tumors are seen in the offsprings (group C). Explain why each of
these mice get/do not get tumors and the nature of those tumors (environmental/inherited).](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2Fd891009c-d394-441a-930b-8d5c1fe8da7b%2F626779ee-99a7-4dc3-9ad8-0d0b92defdbd%2F87brr3v_processed.jpeg&w=3840&q=75)
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- 5b. When you mutagenize a diploid organism, chances are astronomically high that you will be creating a heterozygote on the spot. Why would your mutation be heterozygous and not homozygous?4). p53 (sometimes called TP53 for “tumor protein 53") is a human tumor suppressor gene that is mutated in the majority of human cancers (many tumor types). a. For each of the mutations described below (i-iv): is this a mutation you would expect to find when sequencing p53 alleles from tumor cells? Why or why not? i. A missense mutation encoding a hyperactive form of the protein. ii. A deletion of the gene. iii. An insertion in the promoter that increases transcription 10-fold. iv. A nonsense mutation. b. When sequencing the p53 gene in tumor cells, would you expect to find only mutant version(s) of the gene or a mix of mutant and wild type versions? c. For any of the mutations you said you would expect to find in tumor cells, would you expect tumor cells to be homozygous (same mutation on both chromosomes)? Why or why not? d. Individuals with Li-Fraumeni syndrome have a very high risk of tumors originating in various tissues due to inheritance of a loss-of-function mutant allele of…5. Currently you are studying threonine synthesis in E. coli. To find genes whose protein products are important for threonine synthesis, you perform a mutagenesis to find mutants that require a source of threonine to grow. mtl mt2 mt3 nt4 mt5 mt6 mt7 mt8 mt9 wt You find a total of nine mutants, all of which have recessive phenotypes. You perform complementation tests with all of your mutants. Below are the results for your complementation tests. A (+) means growth and a (- means no growth: mtl mt2 mt3 mt4 mt5 mt6 mt7 mt8 mt9 Wt a. How many complementation groups did you identify? For each complementation group, indicate which mutants belong to that complementation group. ++ I++++ + + + + 主+
- When a particular mutagen identified by the Ames testis injected into mice, it causes the appearance of manytumors, showing that this substance is carcinogenic.When cells from these tumors are injected into othermice not exposed to the mutagen, almost all of the newmice develop tumors. However, when mice carryingmutagen-induced tumors are mated to unexposed mice,virtually all of the progeny are tumor free. Why can thetumor be transferred horizontally (by injecting cells)but not vertically (from one generation to the next)?In the treatment of cancer, the basis for many types of chemotherapyand radiation therapy is that mutagens are more effective at killingdividing cells than nondividing cells. Explain why. What are possibleharmful side effects of chemotherapy and radiation therapy?1.What types of enzymes could Avery, MacLeod, and McCarty have used to destroy proteins and RNAs? 2.Why might Werner syndrome increase the chances of getting cancer? 3.What protein may have been used to detect the telomeres?
- 12 13 14 Which of the following is true of a somatic mutation? A. They are mutations passed on to offspring. B. They occur less often than germline mutations. C. They are mutations in gametes, germ cells or gametocytes. D. They are mutations in cells other than gametes, germ cells or gametocytes. Which of the following best defines a transgenic organism? An organism that has had a portion of its genome deleted An organism that has had a synthetic gene inserted into its genome An organism that has been cross mated with a different organism An organism that has been modified to carry a gene derived from a different organism A. B. C. D. The disease Malaria is caused by Plasmodium. The main structural features of Plasmodium are show below. Nucleus Plasma Membrane Mitochondria K.Quigley 2021 A. Spores. B. Runners C. Binary fission D. Nuclear fusion Polar Ring -Rhoptries Ribosomes From the diagram, what is the most likely method of reproduction used by this organism in the human body?7. Scientists studying the genetics of a congenital discase analyzed the chromosomes of the patient and found a large portion of chromosome twenty-three in 188 Chapter 3. Gene expression and protein synthesis chromosome one, and a small part of chromosome one in chromosome twenty- three. What type of mutation is this? To answer the question, please explain: 1) what the mutation is? 2) what types of mutation do you know?Two genes associated with breast cancer, BRCA1 and BRCA2, were discovered in 1994 and 1995, respectively, and shortly thereafter, were patented by Myriad Genetics, a company based in Utah. Under the patents, testing for mutations in these genes could only be performed by Myriad, at costs from 300 to 3,000. Myriad also patented the process of analyzing the results of such tests, preventing anyone who obtains the sequence of their BRCA genes by other means (which itself would probably be patent infringement) from interpreting the information. The idea that genes can be patented has been a contentious issue from the beginning. Patents are not granted for products of nature, meaning that genes inside the body are not patentable, but biotech companies successfully argued that by removing a gene from the human body, purifying it, and then obtaining its DNA sequence, they created something not found in nature, and which is therefore a patentable invention. The U.S. Patent Office found the argument persuasive, but opponents argue that genes are parts of our bodies and can be identified but not invented. Biotech companies argue that without the protection offered by patents, they would have no incentive for research and development of diagnostic tests. In Europe, patents for BRCA1 and BRCA2 were revoked in 2004 because they did not meet the standards for a patent. After more than a decade of legal disputes, the patents were partially restored in 2008 on a very restricted basis. In the United States, a lawsuit, focused on the patents for the BRCA genes, was filed in May 2009. The suit challenges the basic idea that genes are patentable. In November 2009, the judge ruled that the lawsuit can proceed, and the case is moving forward. In March 2010, a federal court invalidated Myriad Genetics patent on these genes. In August 2011, the U.S. Court of Appeals reversed the lower courts decision and ruled that gene sequences isolated from cells are not a product of nature and are therefore patentable. The case went to the U.S. Supreme Court, which ordered the appeals court to reconsider the case. The Federal Appeals Court did not change its decision, and the case once again, went to the U.S. Supreme Court. A unanimous decision in June 2013 invalidated Myriads patents on the basis that isolating a gene from nature does not make it patentable. This is a landmark decision on gene patenting with widespread ramifications for the biotechnoloogy industry. Will this decision reduce the incentives for companies to invest in new diagnostic tests that would be used by cancer victims or those with serious genetic disorders?
- 9. All organisms have the ability to repair DNA damage caused by mutagenic chemicals. To find genes that encode enzymes that repair DNA damage, scientists isolate mutants that have an abnormally high sensitivity to mutagenic chemicals. Suppose that five different true-breeding mutagen sensitive strains of fruit fly Drosophila melanogaster were isolated (mus mutants). Call these strain #1, strain #2, strain #3, strain #4, and strain #5. Complementation tests were performed with all of these strains and the results are given in the table below. A "+" symbol indicates that when the two indicated strains were crossed, the hybrid was wild-type and a "-" symbol indicates that the hybrid was mutagen sensitive. Assume that each strain has a mutation in just one gene. strain 1 strain 2 + strain 3 + strain 1 strain 2 strain 3 strain 4 strain 5 strain 4 + A. Which mutant strains have mutations in the same gene? B. How many different mus genes are represented here? strain 5 + + + + -1) Create a graph as a better way to display the data in the table 2) Determine which mutations (5q, 18q, 17p, Ras) caused the progression to each stage of tumorigenesis.18) MUTATIONS: A. Explain the difference between a point mutation and a frameshift mutation. B. Explain how the mutation (both a point mutation and frameshift mutation) might impact the production of proteins. C. Name one type of chromosome mutation and explain what it is.
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