Genetics: From Genes to Genomes
6th Edition
ISBN: 9781259700903
Author: Leland Hartwell Dr., Michael L. Goldberg Professor Dr., Janice Fischer, Leroy Hood Dr.
Publisher: McGraw-Hill Education
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Chapter 20, Problem 10P
| a. | Would you expect a cell to continue or to stop dividing at a nonpermissive high temperature if it is a temperature-sensitive Ras mutant whose protein product is fixed in the GTP-bound form at nonpermissive temperature? |
| b. | What would you expect if you had a temperature-sensitive mutant in which the Ras protein stays in the GDP-bound form at high temperature? |
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Chapter 20 Solutions
Genetics: From Genes to Genomes
Ch. 20 - For each of the terms in the left column, choose...Ch. 20 - Characterize the differences between tumor cells...Ch. 20 - Prob. 3PCh. 20 - Prob. 4PCh. 20 - A carcinogenic compound is placed on the skin of...Ch. 20 - You have decided to study genetic factors...Ch. 20 - B cells are specialized blood cells that secrete...Ch. 20 - Molecules outside and inside the cell regulate the...Ch. 20 - Put the following steps in the correct ordered...Ch. 20 - a. Would you expect a cell to continue or to stop...
Ch. 20 - Two different protein complexes called SCF and APC...Ch. 20 - One of the hallmarks of mitotic anaphase is the...Ch. 20 - Concerning the Tools of Genetics Box Analysis of...Ch. 20 - Are genome and karyotype instabilities...Ch. 20 - Prob. 15PCh. 20 - Why dont all loss-of-function mutations that are...Ch. 20 - Chromothripsis is a rare phenomenon, first...Ch. 20 - The chromosome 9/22 translocation associated with...Ch. 20 - A female patient 19 years old, whose symptoms are...Ch. 20 - Prob. 20PCh. 20 - A generic signaling cascade is shown in the...Ch. 20 - Neurofibromatosis type 1 NF1; also known as von...Ch. 20 - Families with germ-line BRCA1 or BRCA2...Ch. 20 - The text explained that retroviruses can cause...Ch. 20 - Hepatocellular carcinoma is the most frequent form...Ch. 20 - Suppose that instead of microarrays, you analyzed...Ch. 20 - Prob. 27PCh. 20 - Glioblastoma multiforme GBM is the most common and...Ch. 20 - a. The legend to Fig. 20.29 identifies which of...Ch. 20 - The website CBioPortal http://www.cbioportal.org...
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- If p63 can bind to the same promoter elements as p53, why would it be considered an inhibitor of p53? Can you clarify this relationship a bit?arrow_forwardWhile investigating the function of a specific growth factor receptor gene from humans, researchers found that two types of proteins are synthesized from this gene. A larger protein containing a membrane spanning domain recognizes growth factors at the cell surface, stimulating a specific downstream signaling pathway. In contrast, a related, smaller protein is secreted from the cell and binds available growth factor circulating in the blood, thus inhibiting the downstream signaling pathway. Speculate on how the cell synthesizes these disparate proteins.arrow_forwardIn addition, when ARF is artificially expressed in normal cells, a rapid increase in p53 levels is observed. Studies have demonstrated that ARF, when expressed, is associated with Mdm2. When associated, the two proteins display a particular pattern of localization restricted to the nucleolus. Suggest a mechanism by which ARF leads to p53 build-up.arrow_forward
- For the Igf2 gene, where do de novo methylation and maintenancemethylation occur?a. De novo methylation occurs in sperm, and maintenancemethylation occurs in egg cells.b. De novo methylation occurs in egg cells, and maintenancemethylation occurs in sperm cells.c. De novo methylation occurs in sperm, and maintenancemethylation occurs in somatic cells of offspring.d. De novo methylation occurs in egg cells, and maintenancemethylation occurs in somatic cells of offspring.arrow_forward. Another class of suppressor mutations, not describedin the chapter, are mutations that suppress missensemutations.a. Why would bacterial strains carrying such missense suppressor mutations generally grow moreslowly than strains carrying nonsense suppressormutations?b. What other kinds of mutations can you imagine ingenes encoding components needed for gene expression that would suppress a missense mutationin a protein-coding gene?arrow_forwardDescribe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?arrow_forward
- ATM is a kinase that phosphorylates histone H2AX in response to double-stranded DNA breaks. Which of the following scenarios would most quickly regulate ATM activity in the cell? a) Adding silencing methyl groups to cytosines in the Atm gene b) Modifying the histone code for the Atm gene c) Increasing expression of a miRNA specific for the Atm mRNA d) Activating an E3 ubiquitin ligase specific for the ATM proteinarrow_forwardCan you please help me by drawing a serie of schematic figures that demonstrates the information in the paragraph below. The carboxy terminus of the p53 protein acts as an allosteric regulator of sequence-specific DNA binding. This was demonstrated initially by Hupp et al. (1992) using a bacterially expressed protein. Recombinant bacterial p53 bound poorly to DNA, and binding could be enhanced by the addition of antibodies specific to the C-terminal region of the protein. Phosphorylation of Ser315 and Ser392 within this domain also enhance sequence-specific DNA binding. Dephosphorylation of Ser376 of p53 after IR allows the association of 14-3-3 proteins with the C terminus of the protein (Waterman et al., 1998). Stavridi et al. (2001) demonstrate that this interaction is required for p53 to activate the downstream gene, p21waf1/cip1, and for the G1 cell cycle checkpoint arrest response. Interestingly, this dephosphorylation event seems to be ATM-dependent, possibly by a phosphatase…arrow_forwardIn a particular organism, there are two similar genes called YFG1 and YFG2. YFG1 is expressed in the liver and not in the pancreas, and YFG2 is expressed in the pancreas but not the liver. Neither YFG1 nor YFG2 is expressed in the heart. If you extract DNA from heart cells, do you expect to see the YFG2 gene? Explain why. Do you expect to see the YFG1 protein when you analyze protein extract from liver cells? And from pancreas cells? And from heart cells? Explain why. Is it possible to produce YFG1 and YFG2 proteins via alternative splicing? Explain one possible way (mechanism) to regulate the expression of YFG1 gene.arrow_forward
- Expression of recombinant proteins in yeast is an important tool for biotechnology companies that produce new drugs for human use. In an attempt to get a new gene X expressed in yeast, a researcher has integrated gene X into the yeast genome near a telomere. Will this strategy result in good expression of gene X? Why or why not? Would the outcome of this experiment differ if the experiment had been performed in a yeast line containing mutations in the H3 or H4 histone tails?arrow_forwardWhich ONE of the following is TRUE concerning the so‐called Philadelphia chromosome? Select one: A.It results in loss of BCR serine‐threonine kinase activity B.It leads to generation of a fusion protein with constitutively active tyrosine kinase activity C.It results from a t(8;21) translocation D.Overexpression of the ABL1 gene results from a translocation that brings a strong gene promoter close to the ABL1 genearrow_forwardThere is a protein called neurogenin that stimulates neuronal cells to differentiate. In order to determine what kind of receptor neurogenin binds to, you add a general phosphatase (one that can remove phosphates from any substrate) to neural cells when you add neurogenin, and you discover that this inhibits differentiation. Furthermore, in the presence of this phosphatase, you find that not even a G protein is activated in response to neurogenin. 1. With this information, what kind of receptor does neurogenin bind to? 2. In a normal cell, how does the G protein in this pathway get activated? 3. In a normal cell, why does the response to neurogenin cease over time?arrow_forward
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