10. ATP synthase is a key enzyme of mitochondrial energy conversion.Mitochondrial ATP synthase deficiency is due to a mutation in a geneimportant for the formation of a subunit in the ATP synthase complex,seen in the illustration below. Scientists could use cells with this genemutation to investigate which of the following questions? (LS1-7) *InnermitochondrialmembranePYRUVATEGLYCOLYSIS ODATIONACOCYCLEOXIDATIVEPHOSPHORYL-ATIONATPsynthaseProtein complexof electronIntermembrane-spacecarriersIIIInnermitochondrialmembraneFADH, FAD2 H* + ½02H,0NADNADH(carrying electronsfrom food)ADP + OАТРMitochondrialmatrixOxidative phosphorylationWhat effect does the mutation have on the movement of electrons between theelectron carriers of the electron transport chain?What effect does the mutation have on the amount of ATP synthesized during cellularrespiration?What effect does the mutation have on the number of protons pumped into theintermembrane space of the mitochondria?What effect does the mutation have on the number of water molecules formed at theend of the electron transport chain?

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Description: 10. ATP synthase is a key enzyme of mitochondrial energy conversion.Mitochondrial ATP synthase deficiency is due to a mutation in a geneimportant for the formation of a subunit in the ATP synthase complex,seen in the illustration below. Scientists c

As the name suggests, oxidative phosphorylation is the formation of ATP by the oxidation of the…

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Biochemistry

10. ATP synthase is a key enzyme of mitochondrial energy conversion. Mitochondrial ATP synthase deficiency is due to a mutation in a gene important for the formation of a subunit in the ATP synthase complex, seen in the illustration below. Scientists could use cells with this gene mutation to investigate which of the following questions? (LS1-7) * Inner mitochondrial membrane PYRUVATE GLYCOLYSS ODATION CITRIC ACO CYCLE ODATIVE PHOSPHORYL ATION ATP synthase Protein complex of electron carriers Intermembrane• space Inner mitochondrial membrane FADH, FAD 2 H* + ½02 H,0 NADH NAD ADP + P ATP (carrying electrons from food) Mitochondrial matrix Oxidative phosphorylation What effect does the mutation have on the movement of electrons between the electron carriers of the electron transport chain? What effect does the mutation have on the amount of ATP synthesized during cellular respiration? What effect does the mutation have on the number of protons pumped into the intermembrane space of the mitochondria? What effect does the mutation have on the number of water molecules formed at the end of the electron transport chain?

10. ATP synthase is a key enzyme of mitochondrial energy conversion. Mitochondrial ATP synthase deficiency is due to a mutation in a gene important for the formation of a subunit in the ATP synthase complex, seen in the illustration below. Scientists could use cells with this gene mutation to investigate which of the following questions? (LS1-7) * Inner mitochondrial membrane PYRUVATE GLYCOLYSS ODATION CITRIC ACO CYCLE ODATIVE PHOSPHORYL ATION ATP synthase Protein complex of electron carriers Intermembrane• space Inner mitochondrial membrane FADH, FAD 2 H* + ½02 H,0 NADH NAD ADP + P ATP (carrying electrons from food) Mitochondrial matrix Oxidative phosphorylation What effect does the mutation have on the movement of electrons between the electron carriers of the electron transport chain? What effect does the mutation have on the amount of ATP synthesized during cellular respiration? What effect does the mutation have on the number of protons pumped into the intermembrane space of the mitochondria? What effect does the mutation have on the number of water molecules formed at the end of the electron transport chain?

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter7: Cellular Respiration: Harvesting Chemical Energy

Section: Chapter Questions

Problem 7TYK

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Some human diseases are caused by mutations in mitochondrialgenes. Which of the following statements is false?a. Mitochondrial diseases may follow a maternal inheritance pattern.b. Mutations associated with mitochondrial diseases often affectcells with a high demand for ATP.c. The symptoms associated with mitochondrial diseases tend toimprove with age.d. Heteroplasmy plays a key role in the severity of mitochondrialdisease symptoms
7. Why are electron carriers (NAD+/NADH and FAD/FADH2) so important in the process of cellular respiration? a) They deliver electrons to the ETC, which in turn sets up chemiosmosis, where most of the ATP is generated. b) They separate the electrons from the protons so that the protons can be moved out of the mitochondrion. c) NADH and FADH2 are major components of the ETC, so without them, there would be no ETC in the cell. d) The electrons that they carry are able to directly phosphorylate ADP in order to generate the bulk of ATP in the cell. e) They transport protons across the mitochondrial membrane.
Some human diseases are caused by mutations in mitochondrialgenes. Which of the following statements is false?a. Human mitochondrial diseases follow a maternal inheritance pattern.b. Mutations associated with mitochondrial diseases oftenaffect cells with a high demand for ATP.c. The symptoms associated with mitochondrial diseases tendto improve with age.d. Heteroplasmy plays a key role in the severity of mitochondrial disease symptoms
1) When a de-coupler such as 2,4-DNP is added to a respiring mitochondrion, which of the following effects on the process of ETC-OP will be true, which will be false. a) Mitochondria no longer reduce O2 to H2 b) Electrons no longer enter the electron transport chain. c) Activity of Complex V (ATP Synthase) is greatly decreased. d) The P/O ratio for FADH2 becomes larger than the P/O ratio for NADH. e) Protons are no longer pumped from the mitochondrial matrix to the intermembrane space. 2) The rate-limiting step in fatty acid synthesis is: a) condensation of acetyl-CoA and malonyl-CoA. b) formation of acetyl-CoA from acetate. c) formation of malonyl-CoA from malonate and coenzyme A. d) the reaction catalyzed by acetyl-CoA carboxylase.
5. a) The cell creates molecules of NADH and FADH2to use in the electron transport chain as they are electron carrier molecules. The electron transfers from these moleculesdrives the movement of what molecule across the mitochondrial membrane?b) What is chemiosmosis?c) How does the cell use chemiosmosis to drive overcome the thermodynamic barrier of bringing phosphates close togehter to create ATP?d) What steps of oxidative phosphorylation are in the cytosol and which are in the mitochondria?e) Cellular respiration can be controlled at the post-translational level. What does this mean, using GLUT as an example? Why is post-translational control of GLUT evolutionarilyadaptive over transcriptional control?f) How does establishment of equillibria of various molecules control metabolic reactions? What are three ways high ATP in the cell control cellular respiration?g) Why are the enzymes controlling the initial steps of various biochemical pathways are targeted by allosteric control?
The catalytic mechanism of an enzyme found in the mitochondrial matrix (pH = 7.8) depends on an active site Lys residue (pKa = 9.5) that acts as a general acid. Mutation of a neighboring residue alters the microenvironment of the Lys side chain so that its pKa shifts from 9.5 to 7.4. (a) Calculate the ratio of protonated to deprotonated Lys at pH 7.8 for the normal and mutant enzyme. (b) Would you expect the mutation to increase or decrease the reaction rate? Explain your answer.(c) Lys is a classified as a basic amino acid, but it commonly acts as an acid catalyst in biochemical reactions. Explain this paradox.
Long term use of high-dosage tetracycline causes cellular damage that mimics mitochondrial disease becauseChoose one :A. mitochondrial proteins are easily denatured by drugs like tetracycline. B. mitochondrial ribosomes are susceptible to inhibition by tetracycline. C. mitochondrial lipid bilayers become leaky due to drugs like tetracycline. D. the mitochondrial inner membrane is solubilized by tetracycline. E. mitochondrial DNA is alkylated by drugs like tetracycline..
The catalytic mechanism of an enzyme found in the mitochondrial matrix (pH = 7.8) depends on an active site Lys residue (pKa = 9.5) that acts as a general acid. Mutation of a neighboring residue alters the microenvironment of the Lys side chain so that its pKa shifts from 9.5 to 7.2. Would the mutation cause the reaction rate to increase or decrease? Explain your answer.
1 a) What is meant by the ATP currency exchange ratio? Why does the oxidation of mitochondrial FADH2 generate one less ATP than oxidation of mitochondrial NADH? b) If 12 H+ are moved across the inner mitochondrial membrane by NADH oxidation, and each ATP synthesized requires 3 H+ to move through ATP synthase, why are only 3 ATP molecules produced by oxidation of each NADH?
1. Which of the following processes generates the most ATP? (Account for the no. of ATP) a. ) Citric Acid Cycle b.) Fatty Acid oxidation c.) Glycogenolysis d.) Glycolysis e.) Pentose phosphate pathway 2. What is the overall chemical changes that occur during one complete turn of the Krebs cycle? 3. Does the mitochondrial matrix ever run out of protons for pumping in oxidative phosphorylation?
Mitochondrial oxidation of fatty acids is a major source of ATP, yet fatty acids can be oxidized elsewhere. What organelle, besides the mitochondrion, can oxidize fatty acids? What is the fundamental difference between oxidation oc- curring in this organelle and mitochondrial oxidation?
Aerobic respiration, used by the mitochondria of eukaryotic cells, is best represented by which of the following balanced equations? 6CO2 + 12H2S g C6H12O6 + 6S2 + 6H2O C6H12O6 + 6O2 + 6H2O g 6CO2 + 12H2O C12H22O11 + H2O g C6H12O6 + C6H12O6 6CO2 + 12H2O g C6H12O6 + 6O2 + 6H2O C6H12O6 + C6H12O6 g C12H22O11 + H2O