EBK GENETICS: FROM GENES TO GENOMES
6th Edition
ISBN: 9781260041255
Author: HARTWELL
Publisher: MCGRAW HILL BOOK COMPANY
expand_more
expand_more
format_list_bulleted
Concept explainers
Question
Chapter 12, Problem 23P
Summary Introduction
a.
To determine:
The explanation for the results obtained.
Introduction:
The telomerase refers to a ribonucleoprotein that adds a repeat sequence to the 3' end of the telomeres.
Summary Introduction
b.
To determine:
The reason one should be cautious while trying treatments.
Introduction:
The enzyme telomerase is responsible for maintaining the length of the telomeres. The telomerase enzymes add a repetitive guanine-rich sequence to the telomeres.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
a. How do bacteria increase the efficiency of gene expression? Is this possible in eukaryotes?
b. A mutation in the promoter of Gene K disrupts an enzyme binding site and results in the loss of
Gene K expression. Is this change in gene expression likely happening at the transcriptional or the
translational level? Explain.
c. Propose three different mutations to prevent initiation, elongation, and termination of bacterial
transcription, respectively. Explain how/why each mutation would prevent its respective step. (Hint:
mutations can be in genes that encode proteins or regulatory DNA sequences)
Telomerase is an attractive cancer target since 85% - 90% of tumors express telomerase (while normal cells express little to no telomerase). One paradigm in this model is the “cancer stem cell” hypothesis. Cancer stem cells (or tumor-initiating cells with stem-cell like properties) can self-renew, as well as give rise to heterogeneous tumor cell populations (essentially, they are believed to be responsible for the formation and maintenance of the tumor). If these cells are indeed “stem-like” they also divide more slowly, and presumably express telomerase (like normal stem cells).Do you think a treatment strategy that inhibits telomerase would be effective in treating cancer? How does the cancer stem cell hypothesis complicate or compliment these strategies? Justify your answer.
a. How many enhancers were you able to identify with these set of experiments? Explain.
b. If you find any enhancer, in what genetic region, number of base pairs upstream from
MRPA, are they located? Explain.
Chapter 12 Solutions
EBK GENETICS: FROM GENES TO GENOMES
Ch. 12 - For each of the terms in the left column, choose...Ch. 12 - Many proteins other than histones are found...Ch. 12 - What difference exists between the compaction of...Ch. 12 - What is the role of the core histones in...Ch. 12 - a. About how many molecules of histone H2A would...Ch. 12 - The enzyme micrococcal nuclease can cleave...Ch. 12 - a. What letters are used to represent the short...Ch. 12 - About 2000 G bands are visible in a...Ch. 12 - Suppose you performed a fluorescence in situ...Ch. 12 - Which of the following would be suggested by a...
Ch. 12 - For each of the following pairs of chromatin...Ch. 12 - a. Drosophila b. Humans Give examples of...Ch. 12 - One histone modification that is seen consistently...Ch. 12 - Recently, scientists constructed a transgene that...Ch. 12 - Drosophila geneticists have isolated many...Ch. 12 - On the following figures, genes A and B are on the...Ch. 12 - Prob. 17PCh. 12 - The first page of this chapter displays photos of...Ch. 12 - The human genome contains about 3 billion base...Ch. 12 - The mitotic cell divisions in the early embryo of...Ch. 12 - In an experiment published in the journal Cell in...Ch. 12 - a. What DNA sequences are found at the telomeres...Ch. 12 - Prob. 23PCh. 12 - a. In a fluorescent in situ hybridization FISH...Ch. 12 - If you are comparing the two telomeres in each...Ch. 12 - a. What DNA sequences are commonly found at human...Ch. 12 - On the graphs presented in Problem 21, no data is...Ch. 12 - Prob. 29PCh. 12 - Prob. 30PCh. 12 - In the 1920s, Barbara McClintock, later a Nobel...Ch. 12 - Give at least one example of a chromosomal...Ch. 12 - Cornelia de Lange syndrome CdLS is a rare human...Ch. 12 - a. Give at least three examples of types of...Ch. 12 - A number of yeast-derived elements were added to...Ch. 12 - Prob. 36PCh. 12 - The completely synthetic yeast chromosome Syn III...
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
- Consider the following simple regulatory pathways. Assume the full pathway is shown. A- E- B- F- C- G- D- 1 H- A You identify several null mutations (a complete deletion of the gene). For each mutant (ind with a - sign), determine whether the final product (I, J, K or L) is inducible, uninducible, or constitutive. 2 B 3 C 4 D inducible inducible constitutive uninducible constitutive inducible inducible E uninducible F G H > > >arrow_forwardConsider the following simple regulatory pathways. Assume the full pathway is shown. A- E- B- F- C- G- D- 1 A H- 2 B || L You identify several null mutations (a complete deletion of the gene). For each mutant (indicated with a - sign), determine whether the final product (I, J, K or L) is inducible, uninducible, or constitutive. 3 C 4 D inducible inducible constitutive uninducible constitutive inducible inducible E uninducible F G H > I > J Karrow_forwardNegative supercoiling of DNA favors the transcription of genes because it facilitates unwinding. However, not all promoter sites are stimulated by negative supercoiling. The promoter site for topoisomerase II itself is a noteworthy exception. Negative supercoiling decreases the rate of transcription of this gene. Propose a possible mechanism for this effect and suggest a reason why it may occur.arrow_forward
- Cancer cells removed from a patient's tumor have increased gene expression of several hundred genes (including many cancer-causing genes). Scientists determine that the histones from the cancer cells have an overall/average lower affinity for DNA than histones from normal control cells. Which drug is most likely to help treat this patient's cancer? a. An inhibitor for HMT (histone methyltransferases) b. An inhibitor for HDM (histone demethylases) c. An inhibitor for HDACs (histone deacetylases) d. An inhibitor for HATs (histone acetyltransferase)arrow_forwardCancer can be defined as an abnormal proliferation of cells that defy the normal regulatory controls observed by normal cells. Recently, histone deacetylation therapies have been attempted in the treatment of certain cancers [reviewed by Delcuve et al. (2009)]. Specifically, the FDA has approved histone deacetylation (HDAC) inhibitors for the treatment of cutaneous T-cell lymphoma. Explain why histone acetylation might be associated with cancer and what the rationale is for the use of HDAC inhibitors in the treatment of certain forms of cancer.arrow_forwarda. Why is it impossible to induce nonsense mutations(represented at the mRNA level by the triplets UAG,UAA, and UGA) by treating wild-type strains with mutagens that cause only A• G → T• C transitions in DNA?b. Hydroxylamine (HA) causes only G• C → A• T transitions in DNA. Will HA produce nonsense mutations inwild-type strains?c. Will HA treatment revert nonsense mutations?arrow_forward
- A. A mutation is recovered in the gene that encodes the lactose operon repressor protein (LacI). Which of the following lac phenotypes would lead to the conclusion that the mutation causes an inability of the repressor to bind lactose? The lac structural genes would never be expressed. The lac structural genes would be expressed continuously. The lac structural genes would be expressed efficiently only in the absence of lactose. The lac structural genes would be expressed efficiently only in the presence of lactose. B. A mutation is recovered in the gene that encodes the lactose operon repressor protein (LacI). Which of the following lac phenotypes would lead to the conclusion that the mutation causes an inability of the repressor to bind Operator DNA? The lac genes would be expressed efficiently only in the presence of lactose. The lac genes would be expressed efficiently only in the absence of lactose. The lac genes would never be expressed. The lac genes would be…arrow_forwardAfter the initial Actualization of the Cit+ phenotype, there was another alteration to the A-3 genome that resulted in increased growth (e.g. Refinement). What explained the increase in growth rate in response to Refinement? A. Increase number of transporters localized to the plasma membrane. B. Increased ability to metabolize glucose. C. Increased citric acid cycle activity. D. Altered promoter activity resulting in constitutive gene expression.arrow_forwardIf the lacl gene is mutated so that the repressor protein no longer binds to lactose, what will be the effect on the expression of B-galactosidase in lactose's presence and absence? Explain. If the promoter for lacl is mutated so that the expression of the repressor increases, what will be the effect on the expression of B-galactosidase in the presence and absence of lactose? Explain. D. (Extremely tricky question!) Describe the behavior of the lac operon assuming that the lacl gene has been mutated so that the repressor now binds to DNA in the presence of lactose but cannot bind to DNA in the absence of lactose.arrow_forward
- Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…arrow_forwardTumor cells from a person with leukemia have been analyzed to determine which oncogene is involved in the transformation. After partial sequencing of the gene, the predicted gene product is identified as a tyrosine kinase. Which of the following proteins would most likely be encoded by an oncogene and exhibit tyrosine kinase activity? A. Nuclear transcriptional activator B. Epidermal growth factor C. Membrane-associated G protein D. Platelet-derived growth factor E. Growth factor receptorarrow_forwardExplain how a transcriptional fusion to a reporter gene, combined with site directed mutagenesis, can indicate key nucleotides in a regulatory region. Name one in vitro technique that can be used to further confirm the significance of these regions.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:PEARSON
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Anatomy & Physiology
Biology
ISBN:9781259398629
Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:9780815344322
Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:9781260159363
Author:Martin, Terry R., Prentice-craver, Cynthia
Publisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Biology
ISBN:9781260231700
Author:Sylvia S. Mader, Michael Windelspecht
Publisher:McGraw Hill Education
Mitochondrial mutations; Author: Useful Genetics;https://www.youtube.com/watch?v=GvgXe-3RJeU;License: CC-BY