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Answers to End-of-Chapter Questions – Brooker et al ARIS site Chapter 14 Test Yourself Questions 1. Point mutations that do not alter the amino acid sequence of the resulting gene product are called _____________ mutations. a. frameshift b. natural c. silent d. nonsense e. missense Answer: c. Silent mutation do not alter the polypeptide chain. 2. Some point mutations will lead to an mRNA that produces a much short polypeptide. This type of mutation is known as a __________ mutation. a. neutral b. silent c. missense d. nonsense e. chromosomal Answer: d. Nonsense mutation change a normal codon to a stop codon, resulting in a shorter polypeptide chain. 3. The type of mutation that alters the entire amino acid sequence from the site of the mutation is known as a __________ mutation. a. neutral b. silent c. missense d. nonsense e. frameshift Answer: e. Frameshift mutation are caused by the insertion or deletion of nucleotides. This changes the reading frame of the gene and thus the entire amino acid sequence from the point of the mutation. 4. Mutagens can cause mutations by a. chemically altering DNA nucleotides. b. disrupting DNA replication. c. altering the genetic code of an organism. d. all of the above. e. a and b only. Answer: e. Mutagens can chemically or physically alter the DNA, thus changing the nucleotide sequence in existing or newly synthesized DNA molecules. 5. The mutagenic effect of UV light is a. the alteration of cytosine bases to adenine bases. b. the formation of purine dimers that interfere with genetic expression. c. the breaking of the sugar-phosphate backbone of the DNA molecule. d. the formation of pyrimidine dimers that disrupt DNA replication. e. the deletion of thymine bases along the DNA molecule. Answer: d. UV light causes the formation of pyrimidine dimers. During replication, DNA polymerase is likely to cause a mismatch when reading the area of the DNA strand with a thymine dimer. 6. The Ames test a. provides a way to determine if any type of cell has experienced a mutation. b. provides a way to determine the mutagenic effect of certain types of agents. c. allows researchers to experimentally disrupt gene activity by causing a mutation in a specific gene. d. provides a way to repair mutations in bacterial cells. e. all of the above. Answer: b. The Ames test determines the mutagenic effects of certain agents. 7. Xeroderma pigmentosum a. is a genetic disorder that results in uncontrolled cell growth. b. is a genetic disorder where normal NER systems are not fully functional. c. is a genetic disorder that results in the loss of pigment in certain patches of skin. d. results from the lack of DNA polymerase proofreading. e. both b and d. Answer: b. XP is the result of defects in NER system proteins. 8. During mismatch repair, the parental strand is distinguishable from the new strand by a. the lack of mutations in the parental strand. b. the presence of methyl groups on the new strand. c. the presence of methyl groups on the parental strand. d. the 3’ to 5’ orientation of the strand. e. the AUG codon on the new strand. Answer: c. The parental strand is detectable by the presence of methyl groups. 9. Cancer cells are said to be metastatic when they a. begin to divide uncontrollably. b. invade healthy tissue. c. migrate to other parts of the body. d. cause mutations in other healthy cells. e. all of the above. Answer: c. The term metastasis refers to the migration or movement of cancer cells to other parts of the body. 10. Oncogenes are a. mutations in genes that normally inhibit the progression of a cell through the cell cycle. b. mutations that cause the overexpression of genes that normally stimulated cell division. c. viruses that cause cancer. d. mutations in genes that cause metastasis. e. all of the above. Answer: b. Oncogenes are mutated forms of proto-oncogenes. Normally, proto-oncogenes stimulate cell division. However, mutations to oncogenes result in overactive expression of these genes and uncontrolled cell growth. Conceptual Questions 1. Explain the difference between a missense mutation and a nonsense mutation. Answer: A missense mutation is a base substitution that changes a single amino acid in the polypeptide. A nonsense mutation involves a change from a normal codon to a stop codon. 2. Explain how a frameshift mutation can lead to premature termination of a polypeptide. Answer: Because an insertion or a deletion causes a frameshift, the codons following the frameshift are read in different groupings than in the original gene. Because 3 of the 64 codons code for stop codons, there is about a 1 in 21 (around 5%) chance that the new groupings will code for stop codons. When a stop codon is encountered during protein synthesis, the polypeptide terminates. 3. Define oncogene, tumor suppressor gene and proto-oncogene. oncogene: A type of mutant gene that causes the gene to be overactive, thus contributing to uncontrolled cell growth and promoting cancer. tumor suppressor gene: A gene that when normal (that is, not mutant) encodes a protein that prevents cancer; however, when a mutation eliminates its function, cancer may occur. proto-oncogene: A normal gene that, if mutated, can become an oncogene. Experimental Questions 1. Explain the difference between the opposing views of mutation prior to the Lederbergs’ study? Answer: Some individuals believed that heritable traits may be altered by physiological events. This suggests that mutations may be stimulated by certain needs of the organism. Others believed that mutations were random. If a mutation had a beneficial effect that improved survival and/reproductive success, these mutations would be maintained in the population through natural selection. 2. What hypothesis was being tested by the Lederbergs? What were the results of the experiment? Answer: The Lederbergs were testing the hypothesis that mutations are random events. By subjecting the bacteria to some type of environmental stress, the bacteriophage, the researchers would be able to see if the stress induce mutations or if mutations occurred randomly. The researchers subjected the bacterial colonies to infection by bacteriophages. If mutations were caused by the presence of the phage, the mutations should have occurred on the secondary plates. That result was not obtained. Instead, the mutations occurred before exposure to the phage, on the master plate. The colonies that were resistant to the infection were always located on the same areas of the secondary plates indicating that the mutations occur before the T1 phage was introduced. 3. How did the results of the Lederbergs support the idea that mutations are random events? Answer: When looking at the number and location of colonies that were resistant to viral infection, the pattern was consistent among the secondary plates. This indicates that the mutation that allowed the colonies to be resistant to viral infection occurred on the master plate. The secondary plates introduced the selective agent that allowed the resistant bacteria colonies to survive and reproduce while the other colonies were destroyed. Thus, mutations occurred randomly in the absence of any selective agent. Collaborative Questions 1. Discuss the pros and cons of mutation. Answer: A mutation is a heritable change in the genetic material such as DNA. A mutation can be passed from mother cell to daughter cell or the mutation can occur during sex cell formation and be passed from parent to offspring. Many times the word mutation is associated with negative effects but this is not always the case. Mutation increases the genetic variability of a species. If a mutation is favorable, it will be beneficial to that individual and may increase its reproductive success. Likewise, such favorable mutations may be passed to offspring. Over time, this process may increase the frequency of the mutation in a population. On the other hand, however, most mutations are unfavorable and decrease the survival or reproductive success of individuals. These mutations tend to be eliminated from populations. 2. Discuss three ways that alterations in DNA structure can be repaired. Answer: Direct repair - This occurs when a repair enzyme finds an incorrect structure in the DNA and directly converts it back to the correct structure. Excision repair - In this form of repair, an abnormal nucleotide or base is discovered, and a portion of the strand of DNA, which has the abnormality, is removed. The complementary strand of DNA is used as a template to produce a normal segment of DNA. Mismatch repair - This form of repair recognizes a base mismatch. The daughter strand carrying the mismatch is removed, and the complementary strand of DNA is used to replace the incorrect strand.