You identify a disease of epidermal cells in mice in which Gene A is not expressed.Further analyses reveals that the DNA sequence of Gene A in affected and normal mice is the SAME.Which of the choices below could explain why Gene A is NOT expressed in the epidermal cells of the affectedmice. Select all that apply.Lysine residues are acetylated in Histone tails close to Gene A in normal mice but not in affected miceTyrosine residues are phosphorylated in Histone tails close to Gene A in affected mice but not in normalmiceTyrosine residues are phosphorylated in Histone tails close to Gene A in normal mice but not in affectedmiceLysine residues are acetylated in Histone tails close to Gene A in affected mice but not in normal mice

Gene is the segement of DNA which is responsible for producing the protein.

Answered: You identify a disease of epidermal…

Biology Today and Tomorrow without Physiology (MindTap Course List)

5th Edition

ISBN:9781305117396

Author:Cecie Starr, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Christine Evers, Lisa Starr

Chapter10: Biotechnology

Section: Chapter Questions

Problem 2DID

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Scientists are working to develop gene therapy to treat Batten disease, also known as Late Infantile Neuronal Ceroid Lipofuscinosis (LINCL). This fatal, autosomal recessive neurodegenerative disorder results from a mutation in the gene that codes for the enzyme TPP1 (Tripeptidyl peptidase 1). In the absence of this enzyme, a substance called ceroid lipofuscin accumulates in lysosomes in the brain, resulting in seizures, blindness, decline in cognitive function and motor skills, dementia, and death by the late teens or early 20’s. The TPP1 gene is 6695 bp in length. Think about the characteristics of Batten disease, and then suggest an approach to gene therapy that might be effective for this specific genetic disorder. You may assume that your research team is working in the U.S. and your research is funded by a grant from the National Institutes of Health (NIH). 1. Briefly outline a procedure that you could use to carry out the gene therapy for Batten disease.
Which of these is NOT true of nucleosomes? A. Some post-translational modifications to histone proteins serve as binding sites for transcription factors. B. The position of nucleosomes is fixed on the genome and can not be changed. C. The position and post-translational modifications of histones can be inherited through mitosis. D. The binding between DNA and histone proteins can be disrupted by post-translational modifications.
HDAC's are important enzymes involved in the regulation of Gene expression. This is because a. They create the Z form of DNA by removing acetyl groups from cytosines. b. they create euchromatic structure by adding acetyl groups to cytosine. c. they add methyl groups from histones creating less gene expression. d. they remove acetyl groups from histones creating less gene expression. e. they add methyl groups onto cytosines on DNA and create a heterochromatic structure.
Some animals like C. elegans, do not have 5-methylcytosine, but do have methylated adenine. It is not known that the methylated adenine replaces the function of methylated cytosine, but, if it does, which of the following would you predict? That removing the methyl groups from adenines in C. elegans would increase gene expression That removing the methyl groups from adenines in C. elegans would decrease gene expression That removing the methyl groups from adenines C. elegans would have no effect on gene expression
How does adding a methyl or acetyl group to a histone protein alter gene activity?A. A methyl group turns genes off. An acetyl group loosens histone’s grip and increases gene activation.B. A methyl group turns genes on. An acetyl group tightens histone’s grip and decreases gene activation.C. A methyl group increases the probability of a mutation, whereas an acetyl group decreases the probability.D. A methyl group decreases the probability of a mutation, whereas an acetyl group increases the probability.
Geneticists are studying a malfunctioning protein that causes impaired endothelial cell migration and angiogenesis. They have noticed that the amino acid sequence of the protein is truncated compared to normal controls. The mutated mRNA strand is isolated, and analysis shows a nonsense mutation located near the 3' end of the coding region. The 3' terminal coding sequence of the abnormal mRNA strand is shown below. 5`- AUG-ACC-ACU-CCA-CUG-UUG-UUC-CAA-GGG-GAG-AGC-UAG-GUC-CGG-GGC-GGA-AAA-UUU-UAA-3` Write down the tRNA anticodon responsible for adding the last amino acid?
Examination of the histone modifications of a gene reveals an abundance of histone H3 with lysine 27 modified with a single methyl group. Does this suggest that this gene is activated or repressed? How would your answer change if many lysine 27 residues were modified with three methyl groups each?
Examination of the histone modifications around a gene reveals an abundance of histone H3 with lysine 27 modified with three methyl groups. Does this suggest that this gene is activated or repressed? How would your answer change if many lysine 27 residues were modified with acetyl groups?
You are studying growth factor GFA, which you know stimulates the proliferation of goblet cells in theintestine.Goblet cells are responsible for producing and secreting mucin, a mixture of glycosaminoglycans thatprotects the intestinal wall.Some patients suffering from inflammatory bowel disease (IBD) appear to have fewer goblet cells, thereforeless mucin and less protection from toxins and various other pro-inflammatory factors.These patients also have mutations in the gene encoding the GFA receptor (GFAR) in goblet cells,GFAR is a receptor tyrosine kinase (RTK) that autophosphorylates in response to GFA binding, thusbecoming active.QUESTION:explain what changes in GFAR could be caused by these IBD-associatedmutations and why.
A researcher has identified a mutant strain of yeast whose histones are unable to be acetylated. Which of the following is the MOST reasonable prediction for how the phenotype of this mutant yeast will differ from the phenotype of yeast cells with acetylated histones? A. The mutant will grow more rapidly. B. The mutant will grow much more slowly. C. The mutant will show decreased levels of gene expression. D. The mutant will show increased levels of gene expression.
In the image below, the blue squiggly line represents a folded protein. There are two particular amino acids that are colored red and black in the protein. The structure of each of these two specific amino acids is shown in the indicated box. A mutation occurs in the gene that encodes the protein illustrated above. The result of this mutation is that one of the amino acids above is substituted with another. Specifically, the amino acid whose structure is shaded red above (the one on the left in the illustration) is replaced by the amino acid shown below. Use this information to answer the two questions that follow. Please answer these questions. 1. Based on this description, indicate which type of mutation occurred: missense, nonsense, silent, or indel 2. How would this mutation affect this protein's structure and function? Explain in 2-4 sentences. Be specific, and be sure to include details of these specific amino acids in your response. (I'm giving you the…
Mutations that introduce stop codons cause a number of genetic diseases. For example, from 2% to 5% of the people who have cystic fibrosis possess a mutation that causes a premature stop codon in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). This premature stop codon produces a truncated form of CFTR that is nonfunctional and results in the symptoms of cystic fibrosis. One possible way to treat people with genetic diseases caused by these types of mutations is to trick the ribosome into reading through the stop codon, inserting an amino acid in its place. Although the protein produced may have one altered amino acid, it is more likely to be at least partly functional than is the truncated protein produced when the ribosome stalls at the stop codon. Indeed, geneticists have conducted clinical trials of a drug called PTC124 on people with cystic fibrosis. This drug interferes with the ribosome’s ability to correctly read stop codons (C. Ainsworth.…

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