Campbell Biology
12th Edition
ISBN: 9780135188743
Author: Urry
Publisher: PEARSON
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Chapter 17.2, Problem 3CC
WHAT IF? → Suppose X-rays caused a sequence change in the TATA box of a particular gene's promoter. How would that affect transcription of the gene? (See Figure 17 .9.)
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WHAT IF? Suppose X-rays caused a sequence changein the TATA box of a particular gene’s promoter. Howwould that affect transcription of the gene? (SeeFigure 17.9.)
protein. You create a mouse line with Cas9 under control of a brain-specific enhancer, while the short
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sequence Gene Y in both brain and liver tissue. What would expect in each tissue? You can assume
that the CRISPRICas9 system will impact both copies of Gene Y in cells, and that the first exon of
Gene Y is necessary for Gene Ys function.
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b. Liver: Nonfunctional Gene Y; Brain: Funtional Gene Y
c. Liver: Functional Gene Y; Brain: Nonfunctional Gene Y
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. What is an enhanceosome? Why could a mutation in anyone of the enhanceosome proteins severely reduce thetranscription rate?
Chapter 17 Solutions
Campbell Biology
Ch. 17.1 - Prob. 1CCCh. 17.1 - What polypeptide product would you expect from a...Ch. 17.1 - Prob. 3CCCh. 17.2 - MAKE CONNECTIONS In a research artide about...Ch. 17.2 - What enables RNA polymerase to start transcribing...Ch. 17.2 - WHAT IF? Suppose X-rays caused a sequence change...Ch. 17.3 - There are about 20,000 human protein-coding genes....Ch. 17.3 - How is RNA splicing similar to how you would watch...Ch. 17.3 - Prob. 3CCCh. 17.4 - What two processes ensure that the correct amino...
Ch. 17.4 - Prob. 2CCCh. 17.4 - Prob. 3CCCh. 17.4 - WH AT IF? In eukaryotic cells, mRNAs have been...Ch. 17.5 - What happens when one nucleotide pair is lost from...Ch. 17.5 - MAKE CONNECTIONS Individuals heterozygous for the...Ch. 17.5 - WHAT IF? DRAW IT The template strand of a gene...Ch. 17.5 - Prob. 4CCCh. 17 - Describe the process of gene expression, by which...Ch. 17 - What are the similarities and differences in the...Ch. 17 - What function do the 5' cap and the poly-A tail...Ch. 17 - Prob. 17.4CRCh. 17 - What will be the results of chemically modifying...Ch. 17 - In eukaryotic cells, transcription cannot begin...Ch. 17 - Prob. 2TYUCh. 17 - The anticodon of a particular tRNA molecule is (A)...Ch. 17 - Prob. 4TYUCh. 17 - Which component is not directly involved in...Ch. 17 - Using Figure 17.6, identify a 5' 3' sequence of...Ch. 17 - Prob. 7TYUCh. 17 - Would the coupling of the processes shown in...Ch. 17 - Prob. 9TYUCh. 17 - Prob. 10TYUCh. 17 - scientific inquiry Knowing that the genetic code...Ch. 17 - Prob. 12TYUCh. 17 - Prob. 13TYU
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- Plz do explain.Thanks Question:- Many types of breast cancer have chromosomal translocation mutations. What scenario best describes, what occurs during this type of mutation, causing cells to proliferate abnormally? Chromosomal translocations may place the gene downstream near the promoter region, therefore causing over-expression of the gene The gene may be placed in the transcription start site, downstream of the gene, initiating transcription by recruiting polymerase II Translocation mutations will initiate the transcription of mRNA in the cytoplasm of the cell catalyzing protein synthesis. Chromosomal translocations can sometimes place a gene under the control of a powerful enhancer, upstream.arrow_forwardE30. An electrophoretic mobility shift assay can be used to study the binding of proteins to a segment of DNA. In the experiment shown here, an EMSA was used to examine the requirements for the bind- ing of RNA polymerase II (from eukaryotic cells) to the promoter of a protein-encoding gene. The assembly of general transcription factors and RNA polymerase II at the core promoter is described in Chapter 12 (Figure 12.14). In this experiment, the segment of DNA containing a promoter sequence was 1100 bp in length. The fragment was mixed with various combinations of proteins and then subjected to an EMSA. Lane 1: No proteins added Lane 2: TFID Lane 3: TFIIB Lane 4: RNA polymerase I| Lane 5: TFID + TFIIB Lane 6: TFID + RNA 1 2 4 5 6 polymerase II| Lane 7: TFIID + TFIIB + RNA polymerase I| 1100 bp Explain which proteins (TFIID, TFIIB, or RNA polymerase II) are able to bind to this DNA fragment by themselves. Which transcrip- tion factors (i.e., TFIID or TFIIB) are needed for the binding of…arrow_forward. One way to determine where inside a cell a protein(protein X) normally localizes is to generate a reportergene construct containing: (i) the gene X regulatoryregion and coding sequences, and (ii) coding sequencesfor GFP fused in frame to the 3′ end of the gene Xcoding sequences just before the stop codon. A mousecontaining such a transgene will express a hybrid protein X-GFP only in those cells in which gene X is normally expressed.a. The gene X-GFP fusion gene described could begenerated by knocking in GFP coding sequencesinstead of by random insertion of a transgene.Diagram the knockin construct you could use forthis purpose.b. What might the advantage be of the knockin strategy versus the transgene strategy?arrow_forward
- . One mechanism by which antisense RNAs act as negative regulators of gene expression is by base pairingwith the ribosome binding site on the sense mRNA toblock translation. In a second, alternative mechanism,the act of transcribing an antisense RNA can somehow prevent RNA polymerase from recognizing thesense promoter for the same gene. Design an experimental approach that would enable you to distinguishbetween these two modes of action at a specific gene.(Hint: What would be the outcome in each case ifhigh levels of the antisense RNA were transcribedfrom a gene on a plasmid?)arrow_forward. Discuss how mutations may arise in DNA, and the potential consequences for gene function if a point mutation were to occur in (a) the coding region of a gene, and (b) the non-coding regulatory region of a gene.arrow_forward. Let’s say that you have incredible skill and can isolate the white and red patches of tissue from the Drosophila eyes shown in Figure 12-24 in order to isolate mRNA from each tissue preparation. Using your knowledge of DNA techniques from Chapter 10, design an experiment that would allow you to determine whether RNA is transcribed from the white gene in the red tissue or the whitetissue or both. If you need it, you have access to radioactive white-gene DNAarrow_forward
- E32. In the technique of DNase I footprinting, the binding of a protein to a region of DNA protects that region from digestion by DNase I by blocking the ability of DNase I to gain access to the DNA. In the DNase I footprinting experiment shown here, a researcher began with a sample of cloned DNA 400 bp in length. This DNA contained a eukaryotic promoter for RNA polymerase II. The assembly of general transcription factors and RNA polymerase II at the core promoter is described in Chapter 12 (see Figure 12.14). For the sample loaded in lane 1, no proteins were added. For the sample loaded in lane 2, the 400-bp fragment was mixed with RNA polymerase II plus TFIID and TFIIB. 2 400 350 250 175 50 Which region of this 400-bp fragment of DNA is bound by RNA polymerase II and TFIID and TFIIB? || III ||| | ||||arrow_forward. Recall that the trp operon has a special leader sequence (trpL) between the operator and the structural genes that offers attenuation as a mechanism for regulation of gene expression. (A) Draw a diagram of a trpL region of the operon when tryptophan is abundant in the cell.Label the following features: the DNA, 5’ and 3’ polarity of the RNA, the regions 1, 2, 3,and 4 and poly-U of the RNA, the pair of Trp codons (UGG), the ribosome, and RNA-Pol,along with any stem-loop structure that would form under these conditions (B) In the above example, will the rest of the trp operon genes be expressed? Briefly describe your reasoning why or why not (C) The trp codons in region 1 of the trpL gene have mutated to cysteines (UGG to UGC). What will be the effect on attenuation gene regulation of the trp operon? Brieflyexplain your reasoning.arrow_forward4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'...TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3' 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' * promoterarrow_forward
- Based on the given scenario, tell whether structural genes are expressed (YES) or not expressed (NO) 1. LacY is deleted (YES/NO) 2. LacI is deleted (YES/NO) 3. TrpR is deleted (YES/NO) 4. Promoter sequence is deleted (YES/NO) 5. lactose is present in the environment; glucose is absent (YES/NO) 6. tryptophan is absent in the environment (YES/NO) 7. operator is deleted (YES/NO)arrow_forwardQ. Deletion of a single AT base pair from codon number 4 can cause a frameshift mutation in a protein-coding gene. Which of the following additional mutations will restore the reading frame back to “normal” such that the original stop codon will still function? (Note that the amino acid sequence will not necessarily be restored back to normal). Adding a base pair into each of the next two codons. Adding a GC base pair back in where the AT pair was deleted. Adding one base to the next codon and deleting one base from the one after that. Deleting a base pair from each of the next two codons. A. 1,2 and 3 B. 1 and 3 C. 2 and 4 D. 4 only E. All of 1,2,3 and 4 are correctarrow_forward4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3'...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5’ promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above). ii. Mutant B has a 2 G/C pairs inserted between position 19 and 20 (position denoted by the ^ in the sequence above).arrow_forward
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