Biology 2e
2nd Edition
ISBN: 9781947172517
Author: Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher: OpenStax
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Chapter 16, Problem 27CTQ
In cancer cells, alteration to epigenetic modifications turns off genes that are normally expressed. Hypothetically, how could you reverse this process to turn these genes back on?
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Chapter 16 Solutions
Biology 2e
Ch. 16 - Figure 16.5 In E. coli, the tip operon is on by...Ch. 16 - Figure 16.7 In females, one of the two X...Ch. 16 - Figure 16.13 An increase in phosphorylation levels...Ch. 16 - Control of gene expression in eukaryotic cells...Ch. 16 - Post-translational control refers to: regulation...Ch. 16 - How does the regulation of gene expression support...Ch. 16 - If glucose is absent, but so is lactose, the lac...Ch. 16 - Prokaryotic cells lack a nucleus. Therefore, the...Ch. 16 - The a/a operon is an inducible operon that...Ch. 16 - What are epigenetic modifications? the addition of...
Ch. 16 - Which of the following are true of epigenetic...Ch. 16 - The binding of _____ is required for transcription...Ch. 16 - What will result from the binding of a...Ch. 16 - A scientist compares the promoter regions of two...Ch. 16 - Which of the following are involved in post...Ch. 16 - Binding of an RNA binding protein will the...Ch. 16 - An unprocessed pre-mRNA has the following...Ch. 16 - IS. Alternative splicing has been estimated to...Ch. 16 - Post-translational modifications of proteins can...Ch. 16 - A scientist mutates elF-2 to eliminate its GTP...Ch. 16 - Cancer causing genes are called transformation...Ch. 16 - Targeted therapies are used in patients with a set...Ch. 16 - Name two differences between prokaryotic and...Ch. 16 - Describe how controlling gene expression will...Ch. 16 - Describe how transcription in prokaryotic cells...Ch. 16 - What is the difference between a repressible and...Ch. 16 - In cancer cells, alteration to epigenetic...Ch. 16 - A scientific study demonstrated that rat mothering...Ch. 16 - Some autoimmune diseases show a positive...Ch. 16 - A mutation within the promoter region can alter...Ch. 16 - What could happen if a cell had too much of an...Ch. 16 - A scientist identifies a potential transcription...Ch. 16 - Describe how RBPs can prevent miRNAs from...Ch. 16 - How can external stimuli alter...Ch. 16 - Protein modification can alter gene expression in...Ch. 16 - Alternative forms of a protein can be beneficial...Ch. 16 - Changes in epigenetic modifications alter the...Ch. 16 - A scientist discovers a virus encoding a Protein X...Ch. 16 - New drugs are being developed that decrease DNA...Ch. 16 - How can understanding the gene expression pattern...
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- A research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.arrow_forwardImatinib is an anti-cancer drug that inhibits the function of CD117, a receptor protein coded for by the KIT gene. Mutations in the KIT gene are implicated in gastrointestinal cancers. Aimee, who has a gastrointestinal tumor asked her doctor if she could try Imatinib, but her doctor first required that she get a biopsy of her tumor. Hair loss is a well-known side effect of chemotherapy; why does this side effect occur? (1) Chemotherapy targets cells undergoing division. Hair stem cells are constantly replenishing (growing) just like cancer cells. They are then also targeted by chemotherapy, causing hair loss. (2) Chemotherapy targets all cells, whether dividing or not dividing, and hair cells are collateral in the fight against cancer (3) Chemotherapy targets proteins in our cells and hair cells have an abundance of proteinsarrow_forwardSeveral research studies are under way that involve the use of genetherapies to inhibit the growth of cancer cells. Oncogenes are mutant genes that are overexpressed and cause cancer. New gene therapies are aimed at silencing oncogenes by producing antisense RNA that recognizes the mRNAtranscribed from oncogenes. Based on your understanding of antisense RNA , explain how this strategy would prevent the growth of cancer cells.arrow_forward
- You are interested in studying a novel gene that appears to be involved in cancer. There is no information about the function of this gene. What would you do to obtain the cDNA for this gene? How would you express this gene and what expression systems might you utilize to study its function and why? How would determine the subcellular localization of this gene in eukaryotic cells? What are alternative methods in case one doesn't work? How would you purify and determine the 3-dimensional structure of this protein?arrow_forwardIn a qPCR experiment, you find that the mRNA for the gene CDK1 goes down (decreased expression) when you treat your cells with doxorubicin. You wonder whether this is due to epigenetic changes on the gene for CDK1. Name two methods that you might use to check whether there are changes in epigenetic modifications (e.g. DNA methylation or histone tail modifications) on the CDK1 DNA.arrow_forwardWhat is the key difference between cis- and trans-epigenetic mechanisms for maintaining an epigenetic modification? We considered genomic imprinting of the Igf2 gene, in whichoffspring express the copy of the gene they inherit from their father,but not the copy they inherit from their mother. Is this a cisora trans-epigenetic mechanism?arrow_forward
- During certain stages of cell growth, the requirement for certain gene products may require gene amplification. What purpose does gene amplification serve?arrow_forwardsiRNAs are used to “knockdown” gene expression in research. Imagine you are a scientist who hopes to study several genes related to cancer. Select all the scenarios you will be able to successfully use RNA interference with the use of siRNAs (select all that apply): Group of answer choices Regulate transcript levels by targeting the siRNA to core promoter regions (e.g. TATA box) of tumor suppressor genes Regulate transcript levels by targeting the siRNA to the regulatory promoter regions (e.g. enhancers) of tumor suppressor genes Regulate transcript levels by targeting the siRNA to any region of the processed mRNA Regulate transcript levels by targeting the siRNA to the 5’ UTR of the processed mRNA Regulate transcript levels by targeting the siRNA to the 3’ UTR of the processed mRNA Regulate transcript levels by targeting the siRNA to sites where the histone acetyl transferase will acetylate the histones Regulate transcript levels by targeting the siRNA to where the start…arrow_forwardWhich of the following statements concerning enhancer DNA sequences is true? Group of answer choices Enhancer DNA sequences must be located before (upstream) the genes they control. Enhancers DNA sequences are close to the genes they activate (via looping) even if they very far away as measured through the linear DNA sequence. Enhancer DNA sequences will not recruit their respective protein factors if you artificially insert the enhancer backwards. All these statements are true.arrow_forward
- Which of the following is not a possible outcome of changing the epigenetic code? a) exposure of regulatory region b) binding of transcription factors c) altered gene expression d) repositioning of nucleosomes by polymerasesarrow_forwardMany currently marketed drugs exert their pharmacological effects by binding to ligand-activated transcription factors and modulating gene expression. One example, are various drugs that target the estrogen receptor to treat breast cancer, osteoporosis and post-menopausal symptoms. Below is a ChIP experiment examining the effects of no drug treatment (C), the natural hormone estrogen (E) and the drugs tamoxifen (T) and raloxifene (R) on recruitment of coactivators (SRC-1 and CBP), Histone Deacetylase Complexes (HDACs) and acetylation of histones associated with the C-myc gene. Which of the following statements are correct based on this data (select all that apply)?arrow_forwardwhich of the following correctly describes how protein kinase A can activate genes? A: nuclear protein kinase A is activated by cAMP to phosphorylate general transcription factors B: cytosolic protein kinase A is activated by cAMP to release the catalytic subunits, which move into the nucleus and phosphorylate CREB C: cytosolic protein kinase A is activated by cAMP to release the catalytic subunits, which move into the nucleus and phosphorylate general transcription factors D: G protein-coupled receptors may be desensitized by serine phosphorylationarrow_forward
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