bich 2 exam 3 Flashcards
Draw the malate-aspartate shuttle
On doc
Draw the glycerophosphate shuttle
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Name the electron transport proteins in order
Glycerophosphate Dehydrogenase (part of glycerophosphate shuttle) Complex I, Complex III, Complex II, Complex IV
Draw the electron transport chain with the flow of electrons and proton
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Draw the Q cycle
on doc
Why does the q cycle run twice for UQH2?
In the first half-cycle, a ubiquinol molecule attaches onto complex III and transfers the two electrons to the cmplex.
In the second half-cycle of the Q cycle, another ubiquinol attaches onto complex III. Upon binding, the two protons are moved into the intermembrane space and the two electrons follow the same pathways as before.
Describe the Mitchell chemiosmotic theory
Proposed that energy derived from electron transport is stored as an electrochemical potential (pH and
Electrical gradient), which is used as energy to synthesize ATP from ADP and Pi.
How did Racker and Stoekenius confirm Mitchell’s hypothesis?
Reconstitution experiment: generated lipid vesicles containing
bacteriorhodopsin (a light-driven proton pump) and bovine
mitochondrial F0F1 ATP synthase
How does the F1-F0 ATP Synthase work?
Protons enter through the A subunit and bind a c-subunit. This rotates the c ring. One proton binds to each subunit, pushing it to rotate in a complete circle
Protons then exit through the A subunit back into the matrix
The stalk rotates with the c=ring and the stalk hits the alpha/beta subunits causing these subunits to change conformation
Draw a model of the F0F1 ATP synthase and how does it work?
on doc
How do uncouplers affect the proton gradient and ATP production?
Uncoupler: protein or chemical that dissipates the proton gradient as heat
How the light harvest complex (LHC) works and how energy is absorbed and passed?
Photon strikes a pigment molecule in the LHC, excites an electron to a higher energy level. Pigments arranged so they have different absorption spectrum and can capture different wavelengths.
Once excited: the energy from the absorbed photon is quickly transferred between pigments (called resonance energy transfer), where the excited electron in one pigment induce excitement in neighboring pigments until it reaches a reaction center.
At reaction center: contains chlorophyll P680 in PII or P700 in PI they become excited and release high energy electrons into a transport chain.
What happens to electrons that absorb a photon in the Reaction Centers, PSII
PSII: chlorophyll P680. When photon absorbed, it becomes excited leading to the transfer of an electron to an electron acceptor, called pheophytin. The high energy electron goes through an ETC associate with PSII including plastoquinone (PQ), cytochrome b6f and plastocyanin (PC). It pumps protons across the thylakoid membrane from the stroma into the thylakoid lumen. Eventually reach PSI where it replaces an electron that has been excited by another photon.
What happens to electrons that absorb a photon in the Reaction Centers, PSI
contains chlorophyl called P700. The high energy electron is received from PSII and is excited by another photon boosting it to a higher energy level. The excited electron is transferred through a second electron transport chain (ferredoxin (Fd) pathway). The electron passes through ferredoxin and reduces NADP+ to NADPH.
Draw the spatial organization of the proteins and cofactors in photosynthesis
on doc
Draw the electron flow for photosynthesis
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Overall reactions of photosynthesis
6 CO2 + 6 Ribulose 1,5bisP (5-C) —> 12 3-phosphoglycerate (3-C)
—using rubisco
12 3-phosphoglycerate (3-C) —> 1 glucose (6-C) + 6 Ribulose 1,5bisP (5-C)
—-using other calvin cycle enzymes
Net:6 CO2 —> 1 glucose (6-C)
Function of plastocyanin (PC)
Its main function is to transfer electrons from the cytochrome b6f complex (cyt b6f) to photosystem I (PSI).
Plastoquinone (PQ) function
embedded in the thylakoid membrane.
It serves as a mobile electron carrier that shuttles electrons between photosystem II (PSII) and the cytochrome b6f complex (cyt b6f)
Ferredoxin (Fd)
-small iron protein in stoma of chloroplast
-Its primary role is to accept electrons from photosystem I (PSI) and transfer them to various downstream electron acceptors.
- its reaction center chlorophyll (P700), it transfers electrons to ferredoxin, reducing it (Fd^+).
-reduction of NADP+ to NADPH
Draw the Z scheme
on doc
Draw the two reactions of Rubisco
on doc
Why does oxygenase activity decrease plant productivity?
No added carbon so no new carbohydrates. Recycling 2-phosphoglycolate requires ATP
How C4 plants reduce oxygenase activity of Rubisco?
C4 plants: incorporate CO2 into 4-carbon molecule
–Atmospheric CO2is initially incorporated into oxaloacetate
–Tropical grasses, including maize and sugar cane
–Less susceptible to photorespiration
What is the purpose of the Calvin Cycle?
Converts inorganic carbon, CO2 into organic molecules, carbon fixation
What is the function of carnitine palmitoyl-transferase I (CPT-I)
catalyzes the transfer of long-chain fatty acids from CoA to carnitine to form acylcarnitine. (in mitochondrial membrane)
Regulation of CPTI:
Key step in reciprocal regulation of fatty acid catabolism and fatty acid synthesis (to be
discussed later)
Location of fatty acid catabolism in eukaryotic cells
Mainly in the mitochondrial matrix
Draw the Acyl-CoA synthase reaction
on doc
Draw the Beta-oxidation of a saturated fatty acid, one cycly
on doc
Look at the ketone body structures
on doc
Why ketone bodies are produced and what their physiological function is
Produced as a result of the breakdown of fatty acids in the liver when glucose availability is low, such as during fasting, prolonged exercise, or a low-carbohydrate diet.
Why excessive amounts of ketone bodies are produced in untreated Type I diabetes
Insulin is not produced so the glucose uptake is impaired. It seems like there are low levels of glucose due to the lack of insulin which causes increased fatty acid oxidation which goes into the citric acid cycle which exceeds its regulation and these are then converted into ketone bodies.
Function and location of ATP-citrate lyase
Catalyzed the conversion of citrate into acetyl-CoA and oxaloacetate (used in the Krebs cycle)
Located in cytoplasm of eukaryotic cells
Regulation of acetyl-CoA carboxylase
Committed step of fatty acid synthesis
-Inhibitor: Palmitoyl-CoA (negative inhibition feedback)`2 and other fatty acyl-CoA and cAMP dependent phosphorylation
—looks like octamer when inactive
-Activate: citrate (which is determined by isocitrate dehydrogenase (inhibited by ATP and NADH; responds to energy level))
—looks like a chain of octamers when active
isocitrate dehydrogenase
inhibitor: ATP, NADH
Activator: ADP
Regulation of Carnitine palmitoyl-transferase-1
inhibitor: malonyl-CoA
Mechanism of the two step of fatty acid synthesis (MAT, KS)
on doc
Overall reaction sequence for fatty acid synthesis
on doc
What step is the energetic driving for for fatty acid synthesis?
Step 1: with acetyl-carboxylase: converts acetyl-Coa to malonyl-coa
Location of reactions for fatty acid synthesis?
Mostly in cytoplasm besides the production of acetyl co-a and the malonyl-coA shuttle which are in the mitochondria
draw Synthesis of phosphatidic acid and triacylglycerol
on doc
Why did the authors need to delete the gene fadE (acyl-CoA dehydrogenase) when constructing an E. coli strain that produces short-chain alkanes (gasoline)?
FadE is acyl-coA dehydrogenase, which catalyzes the first step in beta oxidation
–Preventing catabolism will result in accumulation of fatty acids in the cells
What types of reactions and what coenzymes would be required to convert fatty acids to gasoline (short-chain alkanes)
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Describe how the activities of FabH and FadD were increased in the engineered E. coli strain (I may ask a question that requires you to understand the biochemical and genetic concepts that were used; you will not need to mention specific details, like which other genes were altered or how a plasmid was constructed)
FadD: Increased its expression levels to maximize the amount of acyl-CoA available for the next step
-Changed the promoter of the gene to increase transcription (not
sufficient)
* Put another copy of fadD on a plasmid overexpress the gene so
more of the enzyme would be made
FadH: FabH does the first keto-synthase step between malonyl-CoA and acetyl-CoA
–FabH is inhibited by unsaturated fatty acids, so it is more active when FadR is deleted
What does MAT, ACP, and KS mean in fatty acid synthesis?
MAT: malonyl-CoA/acetyl CoA transacetylase
ACP:: Acyl Carrier protein
KS: beta-keto acyl synthase (elongates fatty acids)
