Essentials of Genetics (9th Edition) - Standalone book
9th Edition
ISBN: 9780134047799
Author: William S. Klug, Michael R. Cummings, Charlotte A. Spencer, Michael A. Palladino
Publisher: PEARSON
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Textbook Question
Chapter 14, Problem 18PDQ
Human equivalents of bacterial DNA mismatch repair proteins are subject to mutational damage just as are other proteins. What evidence indicates that mutations in human DNA mismatch repair genes are related to certain forms of cancer?
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The figure below summarizes the results of an experiment evaluating the role of Ku80 gene DNA repair. The Ku80 Knock Out mice were generated by genetically deleting the Ku80 gene and the effects of ionizing radiation on lifespan were evaluated. Briefly explain why Ku80 deletion has the observed effects. What form of DNA damage is causing the reduced lifespan and which repair mechanism appears to be responsible for repair of these lesion in normal mice?
With age, somatic cells are thought to accumulate genomic "scars"as a
result of the inaccurate repair of double-strand breaks by non
homologous end-joining (NHEJ). Estimates based on the frequency of
breaks in primary human fibroblasts suggest that by age 70 each human
somatic cell may carry some 2000 NHEJ-induced mutations due to
inaccurate repair. If these mutations were distributed randomly around
the genome, how many genes would you expect to be affected? Would
you expect cell function to be compromised? Why or why not? (Assume
that 2% of the genome - 1.5% coding and 0.5% regulatory - is crucial
information.)
(a) How does the duplication of individual genes occur?
(b) individual that inherit a genetic condition known as xeroderma pigmentosum exhibit an extreme sensitivity to sunlight exposure and often develop skin cancer by the age of 10. What repair pathway is most likely disrupted as a result of such mutation? Explain why?
Chapter 14 Solutions
Essentials of Genetics (9th Edition) - Standalone book
Ch. 14 - CASE STUDY| Genetic dwarfism Seven months...Ch. 14 -
CASE STUDY | Genetic dwarfism
Seven months...Ch. 14 -
CASE STUDY| Genetic dwarfism
Seven months...Ch. 14 - CASE STUDY | Genetic dwarfism Seven months...Ch. 14 -
HOW DO WE KNOW?
1. In this chapter, we focused on...Ch. 14 - Review the Chapter Concepts list on page 257....Ch. 14 - What is a spontaneous mutation, and why are...Ch. 14 -
4. Why would a mutation in a somatic cell of a...Ch. 14 - Why is a random mutation more likely to be...Ch. 14 - Most mutations in a diploid organism are...
Ch. 14 - What is meant by a conditional mutation?Ch. 14 -
8. Describe a tautomeric shift and how it may...Ch. 14 - Contrast and compare the mutagenic effects of...Ch. 14 - Why are frameshift mutations likely to be more...Ch. 14 - Why are X rays more potent mutagens than UV...Ch. 14 -
12. DNA damage brought on by a variety of natural...Ch. 14 - Contrast the various types of DNA repair...Ch. 14 -
14. Mammography is an accurate screening...Ch. 14 - Describe how the Ames test screens for potential...Ch. 14 - What genetic defects result in the disorder...Ch. 14 - In a bacterial culture in which all cells are...Ch. 14 - Human equivalents of bacterial DNA mismatch repair...Ch. 14 - A number of different types of mutations in the...Ch. 14 -
20. Some mutations that lead to diseases such as...Ch. 14 - In maize, a Ds or Ac transposon can cause...Ch. 14 -
22. Presented here are hypothetical findings from...Ch. 14 -
23. Cystic fibrosis (CF) is a severe autosomal...Ch. 14 -
24. Electrophilic oxidants are known to create...Ch. 14 - Skin cancer carries a lifetime risk nearly equal...Ch. 14 -
26. The initial discovery of IS elements in...Ch. 14 -
27. It is estimated that about 0.2 percent of...Ch. 14 -
28. It has been noted that most transposons in...Ch. 14 - Two related forms of muscular dystrophy–Duchenne...
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- BRCA1 is mutated in a large percentage of hereditary breast and ovarian cancers. BRCA1 protein serves as a key enzyme in repairing DNA double-strand breaks. More than 800 mutations in the BRCA1 are clinically significant. This collection of mutations include missense mutations, small deletions, and large rearrangements that result in a protein with reduced function or no protein product. BRCA1 functions by interacting with a variety of proteins, such as Rb, Myc, cyclin-dependent kinase (CDK), and Rad50/51. Rb is important for cell cycle arrest; Myc is a transcription factor that activates genes required for cell proliferation; activated CDK promotes cell cycle progression; and Rad50/51 proteins facilitate repair of DNA double-strand breaks. How many of the mutations listed below would lead to excessive cell growth when the cell was either homozygous or heterozygous for the mutation? Increased expression of Myc Constitutively active Rad50/51 A null mutation in Rb Continuous production…arrow_forwardBecause the degree of DNA methylation appears to be a relatively reliable genetic marker for some forms of cancer, researchers have explored the possibility of altering DNA methylation as a form of cancer therapy. Initial studies indicate that while hypomethylation suppresses the formation of some tumors, other tumors thrive. Why would one expect different cancers to respond differently to either hypomethylation or hypermethylation therapies?arrow_forwardWhat common mutation occurs in many human cancers? Explain how it can have this effect.arrow_forward
- Describe the role of mismatch repair (MMR) in DNA repair.Why do mutations in MMR proteins increase the risk ofhuman cancer?arrow_forwardAssume that there is a double stranded break on DNA double helix of an eukaryotic cell due to X-ray radiation and it is not repaired. In addition, the cell’s Apaf-1 protein is not expressed due to a null mutation in the Apaf-1 gene. Please discuss the effect of not having Apaf-1 expression in the cell with non-repaired double stranded break.arrow_forwardThere are dozens of common variations of the c-myc gene, which are associated with different types of cancer. Here are 3 variations of part of a sequence of the c-myc gene, located between nucleotides 180 and 201. The original sequence is given to you, as well as the sequences of 3 variations. The mutated nucleotide of each variation is annotated in gray. Use this information (picture) to answer the next two (2) questions 1. Which of the c-myc variations is least likely to cause a change in c-myc function?2. Which variation of c-myc produces a nonsense mutation?arrow_forward
- Upon exposure to pro-inflammatory agents such as TNFA, cells produce reactive oxygen species (ROS), which can react with guanine bases in DNA to generate 8-oxo-G. This modified guanine can participate in Hoogsteen base pairs with adenine, an event that upon DNA replication results in G to T and C to A mutations. Guanine-rich promoter regions are particularly susceptible to this type of ROS-induced DNA damage. OGG1 is a DNA glycosylase that recognizes 8-oxo- G. OGG1 is involved in two processes: base excision repair of 8-oxo-G as well as transcription initiation for pro-inflammatory genes such as Cxcl family members. These transcription events also involve binding of NF-KB to promoters as NF-KB recruitment increases dramatically following OGG1 binding to DNA. TH5487 is a compound that mimics 8-oxo-G structure and binds to the active site of OGG1. Using reverse-transcription PCR (RT-PCR), researchers examined whether increasing levels of TH5487 affected the expression of a…arrow_forwardDNA sequencing has provided data to indicate that cancer cells may contain tens of thousands of somatic mutations, only some of which confer a growth advantage to a cancer cell. How do scientists describe and categorize these recently discovered populations of mutations in cancer cells?arrow_forward(b): How many forms can naturally occurring DNA exist in? Explain how these forms are characterized. What properties of the functional groups determine the binding of DNA with anti-cancer agents? Explain.arrow_forward
- In the replica plate experiment, it shows that mutations are random. However, certain environmental stresses (such as high temperature, high salt, and low pH) can increase the mutation rate. QUESTIONS: Does this indicate that mutations are nonrandom, since they increase in response to cell stressors?arrow_forwardYou are interested in studying resistance to heavy metals and have selected the yeast Saccharomyces cerevisea to conduct your studies. You have recovered a deletion mutant that does not tolerate high concentrations of zinc (grows poorly in zinc containing media ) and have designated the mutant pgz-1 (for poor growth in zinc ). (a) What is the advantage to the type of mutant used in this work? What class of mutagen was likely use to generate pgz-1? ( b) Do you expect the PGZ gene to be expressed in your mutant? Explain.arrow_forwardRetinoblastoma is an extremely rare cancer of the retina in the eye. The disease mainly affects children up to the age of 5 years because it can only occur while the nerve precursor cells are still dividing. In its nonhereditary form, a tumor usually occurs in only one eye; in its hereditary form, multiple tumors develop in both eyes.To explore the basis for these differences, a cDNA clone of the Rb gene was used to probe the structure of the gene in cells from normal individuals and from individuals with nonhereditary or hereditary retinoblastoma. As shown in the figure Part A, normal individuals have four restriction fragments (A, B, C, and D) that hybridize to the Rb cDNA probe, indicating that each restriction fragment encodes at least one Rb exon. Samples from fibroblasts and tumor cells of affected persons show some differences in the patterns of hybridization, with some bands missing entirely and some bands present at half intensity. The order of the restriction fragments in the…arrow_forward
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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