Biological Science (6th Edition)
6th Edition
ISBN: 9780321976499
Author: Scott Freeman, Kim Quillin, Lizabeth Allison, Michael Black, Emily Taylor, Greg Podgorski, Jeff Carmichael
Publisher: PEARSON
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Chapter 9, Problem 14PIAT
PROCESS OF SCIENCE How could you determine if the mitochondrial ETC is affected in DNP-treated mice? Propose an experiment to determine if there is a correlation between life span and ETC activity in mitochondria isolated from mice used in the experiment above.
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Here we utilize a novel, well-characterized, endogenous mitochondrial mutation in the ATP6 gene of Drosophila melanogaster with a nearly complete loss of ATP synthase activity. These Drosophila mutants have a missense mutation in ATP6 (G to A transition resulting in a glycine to glutamate change at position 116 in the protein), the mitochondrial gene encoding subunit 6 of the F1Fo-ATP synthase(complex V of the respiratory chain. ATP6 allows for the hydrogen ion translocation required for the rotation of the Fo motor and the production of ATP from ADP. Drosophila ATP61 mutants model human mitochondrial encephalomyopathy and demonstrate phenotypes associated with degenerative disease, including: reduced longevity, mitochondrial pathology, progressive neural dysfunction, tissue degeneration and locomotor impairment.
ATP61 Drosophila mutants exhibit a stereotyped phenotypic progression that is analogous to the symptomatic progression reported for many human mitochondrial disease…
Predict the outcome of the following hypothetical experiments and be sure to explain and be rational in addition to proposing the probable outcome of the experiment:
-> you alter the Rab-GDI binding site so that it cannot interact with Rab-GDP
-> you have identified a drug that can specifically deplete PI(4)P from the trans-Golgi of the cell. When you treat cells with this drug you hypothesize....
-> while investigating novel anti-cancer drugs you identify a compound that disrupts y-tubulin localization to the centrosome and disperses it throughout the cytosol. Why might this compound be a useful anti-cancer agent?
Explain a mechanism for how a nuclear-encoded protein is targeted to the inner membrane of the mitochondrion. Explain the mechanism for how a nuclear-encoded protein is targeted to the thylakoid membrane.
Describe an experiment that could be conducted to show that there is a targeting system for a nuclear encoded protein that ultimately finds its way to a specific organelle.
Chapter 9 Solutions
Biological Science (6th Edition)
Ch. 9 - Where does the citric acid cycle occur in...Ch. 9 - 2. What does the chemiosmotic hypothesis claim?
a....Ch. 9 - 3. After glucose is fully oxidized by glycolysis,...Ch. 9 - 4. What is the primary function of the reactions...Ch. 9 - Compare and contrast substrate-level...Ch. 9 - If you were to expose cells that are undergoing...Ch. 9 - In step 3 of the citric acid cycle, the enzyme...Ch. 9 - 8. Explain the relationship between electron...Ch. 9 - 9. Cyanide (C=N–) blocks complex IV of the...Ch. 9 - QUANTITATIVE Early estimates suggested that the...
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- Design a set of experiments using chimeric proteins, composed of a mitochondrial precursor protein fused to dihydrofolate reductase (DHFR), that could be used to determine how much of the precursor protein must protrude into the mitochondrial matrix in order for the matrix targeting sequence to be cleaved by the matrix processing protease.arrow_forwardIn our feeding experiment with vermilion/brown and cinnabar/brown mutant flies, we were supposed to use kynurenine or hydroxykynurenine to overcome the enzymatic block in the ommochrome pathway, caused by the vermilion or cinnabar mutations. Which eye color would you expect for each of the two double mutants, if we had supplemented the medium with N-formylkynurenine? Use a diagram of the pathway to explain your answer.arrow_forwardThe biogenesis of functional mitochondria is dependent upon the products of both nuclear and mitochondrial genes, which poses several regulatory and logistical issues. Interestingly, many of the nuclear genes encoding mitochondrial proteins are regulated at the transcriptional level by Myc (activates transcription) and p53 (often represses transcription). Does this make sense? Why or why not?arrow_forward
- The DNA located inside of mitochondria exhibits approximately ten times the mutation rate seen in nuclear DNA. Provide an explanation as to why this is the case and what are the effects of this higher mutation rate of mitochondrial DNA on disease processes?arrow_forwardThrough your biotechnology research project at the Tiger One Brewery, you engineered a glucose transporter in a yeast strain in order to increase its rate of fermentation. Your colleague recorded the glucose uptake data shown below from the yeast strain you developed and to your surprise, you found out that your engineered glucose transporter has three- fold more affinity to glucose compared to the wild-type (native/unmodified) glucose transporter. From the figure below, can you predict the Km of the wild-type glucose transporter? Note: The Vmax of the wildtype and engineered transporters are the same in the experimental setup, and the plot below is the data of your engineered glucose transporter and NOT the wildtype (native/unmodified) transporter. Glucose uptake 100.. 50- 25arrow_forwardComponents of the TIM complexes, the multi- subunit protein translocators in the mitochondrial inner membrane, are much less abundant than those of the TOM complex. They were initially identified using a genetic trick. The yeast Ura3 gene, whose product is an enzyme that is normally located in the cytosol where it is essential for synthesis of uracil, was modified so that the protein carried an import signal for the mitochondrial matrix. A population of cells carrying the modified Ura3 gene in place of the normal gene was then grown in the absence of uracil. Most cells died, but the rare cells that grew were shown to be defective for mitochondrial import. Explain how this selection identifies cells with defects in compo- nents required for import into the mitochondrial matrix. Why don’t normal cells with the modified Ura3 gene grow in the absence of uracil? Why do cells that are defective for mitochondrial import grow in the absence of uracil?Components of the TIM complexes, the multi-…arrow_forward
- Marilyn Houck and Margaret Kidwell proposed that P elements were carried from Drosophila willistoni to Drosophila melanogaster by mites that feed on fruit flies (M. A. Houck et al. 1991. Science 253:1125–1129). What evidence do you think would be required to demonstrate that D. melanogaster acquired P elements in this way? Propose a series of experiments to provide such evidence.arrow_forwardIf you could microinject cytochrome c into the cytosol of wild-type mammalian cell and another set that were mutated to be deficient in Bax and Bakl, what would you expect to happen to the wild-type (normal) cells? What about the mutated cells?arrow_forwardA laboratory in Japan performed a similar experiment on earthworms from different localities of the Japanese archipelago, but instead of linking trypsin activity within worms to anatomical features, they were interested in geographical differences in the ability of the worms to breakdown environmental pollutants using the enzyme polyphenol oxidase. The protocol was similar to the one you used, except that enzyme activity was measured from 100 µl of worm extract. Data obtained are displayed below: Replicate Amount of product liberated over 10 Locality Concentration of total protein in worm extract minutes (pmol) (ug/ml) Hokkaido 1 101 4. 2 87 3 3 107 4 4 88 3. 89 Hon-shu 1 126 2. 2 120 3 3 156 153 119 4 Куu-shu 1 103 99 5 3 94 4 108 3 110 5 Okinawa 1 88 3 90 4 3 96 4 100 112 3 From the data in the table, calculate the specific activity of polyphenol oxidase (in units of umol/min/mg protein) from each locality, presenting the data as mean + standard error (n=5). You only need to show 1…arrow_forward
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