BS 161 Biology Worksheet

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BS 161 Biology Worksheet

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Warming Up to Brown Fat Scientists know how to turn on these fat-combusting cells. Can these energy burners be used to combat obesity? Kerry Grens Oct 8, 2015 Brown fat—the form of adipose tissue that burns, rather than stores, energy—was only recently discovered to exist in adult humans. For decades, researchers knew it was present in rodents, whose brown fat reserves are quite large. But it wasn’t until the advent of PET-CT scans that allowed scientists to finally image brown fat in people, about six years Arrows indicate where most brown fat is found in the ago. human body.WIKIPEDIA, HGG6996 “If we are honest, we still don’t know what the function is of the brown fat, especially in humans,” says Patrick Schrauwen, who, along with his colleagues at Maastricht University in the Netherlands, was one of the first researchers to identify brown fat in adult humans. But scientists do know what the tissue is capable of: chewing up calories. This property has made brown fat a tantalizing target for obesity therapies. The question is, Schrauwen adds, “how do we activate it?” Chill out In animals, researchers had found years ago that cold fires up brown fat, likely to regulate body temperature. So in Schrauwen’s early experiments to look for brown fat in humans, he asked a group of young, male volunteers to sit in a cold room (16° C) for two hours. In this condition, brown fat would light up in the scans, but at room temperature, it was not visible. The results demonstrated that it was possible to manipulate brown fat via cold exposure, but would it be enough to produce any benefits? In 2013, Masayuki Saito of Tenshi College in Japan and his colleagues put cold to the test. The team had a small group of volunteers sit in a cold room (19° C) for two hours each day for six weeks. Not only did PET-CT scans show increased brown fat activity, but the study participants’ body fat mass also dropped by a few percent, while control volunteers showed no such changes. Although cold may be a powerful stimulant for brown fat, “it’s not so feasible,” says Schrauwen. “People are not going to sit for two to three hours per day in a cold room. They don’t have time.” One company is developing cooling clothing people could wear to stimulate their brown fat, but even then, researchers say the key to flipping the switch on brown fat is feeling the chill. “It is extremely uncomfortable,” says Harvard Medical School’s Bruce Spiegelman. “So compliance is an issue.” What scientists like Spiegelman really want to develop is a brown fat medicine. Turn on The beleaguered quest for a fat-burning pill has spanned decades, with few successes and a handful of huge flops (think: methamphetamine given to postpartum women in the 1940s, and fen-phen’s ban in the 1990s after its potentially fatal side effects were exposed). But no drug-development attempts to date have specifically targeted brown fat, leaving room in the imagination for a safe, effective, and long-lasting weight loss medication. There are a number of ways of turn on brown fat by ramping up any of the various players involved in the cells’ activity. For instance, through the binding of a receptor called TGR5, bile acids induce brown fat cells to burn calories. Earlier this year, Schrauwen showed that giving women a pill containing the bile acid chenodeoxycholic acid for two days did indeed up their energy expenditure and brown fat activity. “The results were not spectacularly high,” he says. “They were quite small effects. But if the pharmaceutical industry would design more specific TGR5 agonists, this might be the way to go.” Another target is UCP1, or mitochondrial uncoupling protein 1, which causes brown fat cells to produce energy via heat rather than ATP. Wanzhu Jin at the Institute of Zoology at the Chinese Academy of Sciences in Beijing is screening chemicals in mouse models of obesity in search of those that turn on UCP1. He has been dosing himself with one such promising compound, used in traditional Chinese medicine, for months. So far he hasn’t observed any side effects, but he hasn’t witnessed any weight loss either. Rather than breaking new ground with novel compounds, some researchers are repurposing old drugs known to stimulate players on the brown fat activation path, with an eye toward honing their specificity. Patrick Rensen at Leiden University Medical Center in the Netherlands, for instance, is reviving interest in a weight-loss drug called rimonabant that had already been on the market, but was pulled for psychiatric side effects. Rimonabant is known to effect weight loss by binding a cannabinoid receptor, but the mechanism wasn’t entirely unclear. Rensen and his colleagues last year showed that the drug works by increasing noradrenergic signaling in brown fat when the cannabinoid receptor is turned off. If it were possible to develop a form of rimonabant that couldn’t cross the blood-brain barrier, he says, such a drug might be promising. Also on the drug-repurposing hunt is Aaron Cypess of the National Institute of Diabetes and Digestive and Kidney Diseases. He’s studying β3-adrenergic receptor agonists—drugs known to both turn on brown fat and encourage white fat to release fat into the blood. In the 1980s and ’90s, such drugs had been tested for weight loss in clinical trials, but they didn’t effect significant results, and fell out of favor. But that was before it was recognized that they were acting upon brown fat, says Cypess. “People say, ‘This will never work as an obesity treatment.’ My answer is, ‘We haven’t really seen what this tissue can do, because we haven’t tested in remotely analogous conditions to what we test in our mice.’” Cypess is now experimenting with a β3-adrenergic receptor agonist, mirabegron, which is approved to treat overactive bladder. In January, his team showed that a single, large dose of the drug activated brown fat in adults. The next question is whether chronic activation can produce lasting metabolic or weight benefits. Spiegelman, who is pursuing a number of different brown fat-activating compounds, says drugs that both turn on existing cells’ activities and recruit new brown fat cells will be the most effective. “A number of polypeptide small molecules play some role in the browning/beiging response in vivo,” he says. “Which of these are going to be robust enough to be effective in humans is something we don’t know at this point.” Fat transplant One of the challenges of activating brown fat in people is that adult humans have so little of it to begin with—just a few hundred grams, estimates Rensen. And among overweight and obese individuals, that amount tends to be even smaller. But what if we could boost that volume? Jin has had success transferring brown fat from one animal to another. The recipient mice ended up with better insulin sensitivity, resistance to obesity, and, in the case of already overweight animals, signs of obesity reversal. But he says such an approach would not work in humans. For one, people don’t have the large brown fat depot that mice do. Spiegelman says a transplant would require so much volume that it’d essentially be a surgical procedure. (If a person is willing to undergo surgery for weight loss, he says, she might as well get bariatric.) Rensen, too, has tried implanting brown fat into mice, but without success. He says the trouble is that brown fat is innervated with noradrenergic neurons, and without the nerve cells present among the donor brown fat cells, they turn into white fat. Still, he says, there’s a chance it still might work. “As long as it is not proven it doesn’t work, it’s still promising.” A Massachusetts-based biotech called Energesis Pharmaceuticals is working on a different solution to boosting brown fat. It’s developing a procedure to take a bit of fat precursor cells from a person, grow them in the lab, add a compound to differentiate the cells into brown fat, and reinfuse them back into the patient. “We have very good results in mice,” says Olivier Boss, the firm’s chief scientific officer. Energesis estimates it may be able to test the procedure in humans in 18 months. In the meantime, the company is also screening compounds that activate existing brown fat. In either case, says Boss, metabolic benefits are likely to show up first before any substantial weight loss. “My expectation is that it will be sufficient for a lot of patients [to lose weight]. But it’s going to take time.” Market potential Time is something investors don’t always have, creating a challenge for those wishing to develop a brown fat drug that could treat obesity. Spiegelman founded a company called Ember Therapeutics several years ago, but despite preclinical success with several compounds, he says, its primary investor pulled out and shuttered the company. “We were making good progress, but we weren’t making it fast enough,” he says. “I still believe in” a brown fat therapy. Spiegelman says he’s in discussions with another investor to continue his work on developing a brown fat drug for diabetes and weight loss. Like Boss, however, he acknowledges that obesity may be a tougher nut to crack. “I’m much more optimistic about activation of brown fat for diabetes and fatty liver disease. Whether we can achieve enough weight loss as a monotherapy, that’s a high bar,” Spiegelman says. Studies on activating brown fat in humans are still so new that there aren’t enough data to say one way or another if it’s feasible to stimulate weight loss by turning the cells on. Cypess envisions a therapy that would complement existing strategies, namely, exercise and limiting energy intake. “You’re not going to have a diet-in-a-pill,” he says. But he remains optimistic about the promise of brown fat. “We really haven’t pushed the capacity of brown fat in humans yet.” https://www.the-scientist.com © 1986–2022 THE SCIENTIST. ALL RIGHTS RESERVED. #3 x #1 IMS Mitochondrial Inner Membrane x Electron Transport Chain Matrix ½ O2 H2O x x x x x Energy Transfer Carbon Flow A person loses weight when the carbon atoms from fatty acids: #2 x x Muscle Contraction x Beta-Oxidation ½ O2 H2O x x Citric Acid Cycle Fatty Acids Electron Transport Chain ATP Synthase High levels of ATP cause high levels of O2 because: #4 ATP levels are low when UCP1 is active because: Low levels of ATP cause low levels of O2 because: The low levels of O2 cause low levels of NADH because: The high levels of O2 cause high levels of NADH because: The low levels of NADH cause low levels of fatty acids because: The high levels of NADH cause high levels of fatty acids because: This relates to weight loss because: ATP Synthase BS161 – D2L homework week #4 Due 6/11/2022 by 11:59pm Modeling Energy Transfer and Uncoupling Instructions Model Development In this activity you will be developing a scientific model. This model must fit on the template provided. When finished, take a picture of your model and upload your picture to the D2L homework week #3 dropbox. You should use your notes from previous activities, the textbook, the pre-class activity, and the article “Warming Up to Brown Fat” to develop a model explaining why conditions that uncouple electron transport and ATP synthesis in mitochondria of brown fat cause increased body temperature and reduce body fat mass. 1. The model in box 1 on the template represents fatty acid catabolism in muscles that are contracting. • Solid arrows represent the flow of carbon • Open arrows represent energy transfers. Use figures 7.8, 7.10, and 7.18 in the textbook as guidance. Add names of molecules to the boxes marked with an “x”, identifying only key inputs and outputs of the process. Table 1. Relative consumption of key molecules under different conditions. Process Resting muscles / Molecule consumption Contracting Muscles Activated Brown Fat Inactive Brown Fat O2 high low high NADH high low high Fatty Acid high low high Complete the sentence in the bottom of box 1 to explain how a person loses weight during exercise. 2. Table 1 above gives the relative consumption of key molecules from the model in box 1 in different tissues and under different conditions. If a molecule is being consumed, the levels of that molecule will decrease unless more is made. Use what you know about these inputs in how electron transport / oxidative phosphorylation works and feedback mechanisms in cellular respiration, to explain how ATP and NADH are affected in each case. For example, in contracting muscles… • ATP is hydrolyzed for muscle movements. ATP consumed during muscle contraction is replaced by the ATP produced by ATP synthase. Because ATP synthase depends on the proton gradient, the proton pumps must maintain the proton gradient by pumping protons into the intermembrane space. In order for the proton pumps to function, electrons must move through the electron transport chain. • O2 consumption is high because O2 is being reduced to H2O as it accepts electrons from the electron transport chain. • NADH consumption is high because NADH is being oxidized to provide high-energy electrons to the electron transport chain. • Fatty acid consumption is high because fatty acids are oxidized to produce NADH. Reduction of NAD+ is coupled to the oxidation of fatty acids. • Thus, you “burn” fatty acids as a result of exercise. • Feedback: because high levels of NAD+ have positive feedback on reactions of cellular respiration, more exercise leads to greater consumption of fatty acids. Write an explanation in box 2 for how and why consumption of O2, NADH, and fatty acids is regulated in inactive brown fat as seen in Table 1. Note that inactive brown fat or resting muscles do not consume as much ATP. Review Fig 7.19: Do high levels of ATP speed up or slow down reactions in cellular respiration? 1 BS161 – D2L homework week #4 Due 6/11/2022 by 11:59pm In the mitochondria, if ATP is in high concentrations, protons stop flowing through ATP synthase, and the proton gradient becomes so large that electrons can no longer flow through the electron transport chain. Use this information, the model in box 1, and ideas from feedback inhibition in your explanation. 3. The article “Warming Up to Brown Fat” (Grens, Kerry. “Warming Up to Brown Fat”. The Scientist. LabX Media Group. October 8, 2015. Web. February 9, 2016. https://www.the-scientist.com/news-opinion/warming-up-to-brown-fat34696) describes an unusual protein found only in brown fat called uncoupling protein 1 (UCP1). This protein is a channel in the inner mitochondrial membrane that allows protons to pass through the membrane by facilitated diffusion. Paradoxically, though consumption of O2, NADH, and fatty acids is high in active brown fat, ATP production is low. In box 3, • • • Fill in the boxes marked with an “x” Add arrows and a labeled shape to the diagram to demonstrate the role of UCP1 in brown fat mitochondria Illustrate how the presence of UCP1 affects ATP synthase and levels of ATP 4. The article also discusses the possibilities of activating UCP1 in brown fat as a method of weight loss. In box 4, explain • Why ATP levels are low in activated brown fat • how and why this causes high consumption of NADH, O2 and fatty acids seen in Table 1 o Note: cells require ATP to survive and will therefore try to maintain a certain level of ATP • Why this results in weight loss, including how the mass that is lost from the body during weight loss leaves the body 2 BS 161 – Cells & Molecules Dr. Stephanie S. Pandolfi Lecture #15 Cellular respiration Aerobic respiration, anaerobic respiration, and fermentation 1 Cellular respiration Series of exergonic reactions that  Are oxidations  Are also dehydrogenations  Lost electrons are accompanied by hydrogen ions (protons) Therefore, what is actually lost is a hydrogen atom (1 electron, 1 proton) 2 Cellular respiration Cells harvest energy by breaking bonds and shifting electrons from one molecule to another  Aerobic respiration – consumes organic molecules and O2 and yields ATP  Final electron acceptor = O2  Anaerobic respiration – similar to aerobic respiration  Final electron acceptor is inorganic molecule other than O2  Fermentation – partial degradation of sugars  No O2 3 Cellular respiration Glucose = fuel Many steps 1 glucose may = 32 ATP! Hydrogen transfer Redox reaction  Glucose is oxidized  Oxygen is reduced 4 ATP production The goal of cellular respiration is to produce ATP  Energy is released from oxidation reactions in the form of electrons  Electrons are shuttled by electron carriers (e.g. NAD+) to an electron transport chain  Electron energy is converted to ATP 5 How cells make ATP Cells catabolize organic molecules and produce ATP in two ways:  Substrate-level phosphorylation  Aerobic respiration 6 4 stages of cellular respiration Glycolysis  Glucose  2 pyruvate  2 ATP  2 NADH Pyruvate oxidation  2 NADH citric acid cycle  2 ATP  6 NADH  2 FADH2 Electron transport chain 7 Stage 1: glycolysis Enzymes found in cytosol Energy investment reactions Enzyme 2 molecules of ATP invested  Glucose is phosphorylated twice  Energy payoff reactions One 6-carbon glucose broken into two 3-carbon sugar molecules  3-carbon sugars  pyruvate  4 ATP molecules produced directly (2 net ATP)  Electrons transferred to 2 NADH  2 pyruvate Glucose 8 Transporting electrons Electron path from glucose to oxygen Electron acceptors  Nicotinamide adenine dinucleotide = NAD+  NAD+ + 2H+ + 2e-  NADH + H+  Flavin adenine dinucleotide = FAD  FAD + 2H+ + 2e-  FADH2 Electron transport chain  Stepwise transfer of electrons from one protein to another  Releases small amounts of energy with each transfer 9 Recycling NADH As long as food molecules are available to be converted into glucose, a cell can produce ATP  Continual ATP production results in accumulation of NADH and NAD+ depletion  NADH must be recycled into NAD+  With oxygen • Aerobic respiration  Without oxygen • Anaerobic respiration • Fermentation 10 Pyruvate oxidation For each pyruvate molecule  NAD+ reduced to NADH  Pyruvate converted to acetic acid  Acetyl Coenzyme A (Acetyl CoA) CoA 2 1 3 Acetic acid Pyruvic acid CO2 Acetyl-CoA (acetyl-coenzyme A) Coenzyme A 11 Running totals so far… Glycolysis Pyruvate oxidation Net ATP 2 0 NADH 2 2 FADH2 0 0 CO2 0 2 Citric acid Electron cycle transport TOTAL 12 Stage 3: citric acid cycle Occurs in the mitochondria Each acetyl CoA bonds to a 4C “acceptor” molecule to form a 6-C product 6-C molecule is  Oxidized   NADH CO2 5-C molecule is oxidized & decarboxylated again  Acetic acid ADP 2 CO2 citric acid Cycle Decarboxylated  Output Input 3 NAD+ FAD NADH & CO2 Some energy used to transfer a phosphate group to an ADP molecule to form ATP directly 4-C molecule is oxidized   NADH FADH2 4-C molecule is recycled 13 Running totals so far… Glycolysis Pyruvate oxidation Citric acid Electron cycle transport TOTAL Net ATP 2 0 2 NADH 2 2 6 — 10 FADH2 0 0 2 — 2 CO2 0 2 4 — 6 14 Harvesting energy Series of redox reactions  Release energy  Repositioning electrons closer to oxygen atoms 15 Stage 4: electron transport chain NADH & FADH2 transport electrons from food to transport chains ETCs use this energy to pump H+ ions across mitochondrial membrane O2 pulls those electrons down the chain, causing release of H+ ions H+ ions flow into ATP synthase  Chemiosmosis Each pair of electrons brought by NADH  ~2.5 ATP Each pair of electrons brought by FADH2  ~1.5 ATP 16 Chemiosmosis Most cellular ATP produced by ATP synthase enzyme  Inner mitochondrial membrane  Adds phosphate group to ADP Protons move along concentration gradient through enzyme channel  Energy rotates rotor of enzyme  Mechanical energy  chemical energy (ATP) 17 Cellular respiration energy yield Theoretical energy yields  36 ATP per glucose Actual energy yield  30 ATP per glucose  Reduced yield is due to  “Leaky” inner membrane  Use of the proton gradient for purposes other than ATP synthesis 18 19 Totals Glycolysis Pyruvate oxidation Citric acid Electron cycle transport TOTAL Net ATP 2 0 2 ~28 ~32 NADH 2 2 6 — 10 FADH2 0 0 2 — 2 CO2 0 2 4 — 6 20 Catabolism of proteins and fats Proteins  Broken into amino acids  Deamination  Removing amino group (functional group) from amino acids  Remaining carbon chain enters glycolysis or citric acid cycle  Energy is harvested through electron extraction Fats  Beta (b) oxidation  Triglycerides broken into glycerol + 3 fatty acids  Acetyl groups removed from each fatty acid tail  Acetyl group  acetic acid  acetyl CoA  The respiration of a 6-carbon fatty acid yields 20% more energy than glucose 21 Fermentation Anaerobic respiration  Glycolysis only Hydrogen atoms donated to organic molecules = fermentation  Regenerates NAD+ from NADH Types of fermentation  Bacterial  Ethanol  Lactic acid 22 Ethanol fermentation Yeast cells CO2 removed from pyruvate  Forms acetaldehyde  CO2 is the component of yeast that causes bread to rise H+ transferred from NADH to acetaldehyde  Produces NAD+ and ethanol  Source of ethanol in wine and beer 23 Lactic acid fermentation Animal cells (muscle) H+ transferred from NADH to pyruvate  Produces NAD+ and lactic acid Glycolysis can continue in the presence of glucose Lactic acid can build up and lower blood pH  Denaturation of muscle proteins 24 BS 161 – Cells & Molecules Dr. Stephanie S. Pandolfi Lecture #16 Photosynthesis 1 The basics of photosynthesis Almost all plants are photosynthetic autotrophs (producers), as are some bacteria and protists  They generate their own organic matter through photosynthesis  Atmospheric oxygen due to photosynthesis (a) Mosses, ferns, and flowering plants (c) Euglena (d) Cyanobacteria (b) Kelp 2 Photosynthesis overview Energy of most living cells comes from the sun  Captured by plants, algae, or bacteria  Photosynthesis 2 types of reactions  Light-dependent reactions (the photo part)  Capture energy from sunlight  Use energy to produce ATP and reduce NADP+ to NADPH  Calvin cycle (the synthesis part)  Carbon fixation reactions  Use ATP & NADPH to make organic molecules from CO2 3 Formula for photosynthesis 6CO2 + 12H2O + light  C6H12O6 + 6H2O + 6O2 Water is oxidized and CO2 is reduced Tracking atoms through photosynthesis Reactants: Products: 6 CO2 C6H12O6 12 H2O 6 H2O 6 O2 Leaf anatomy overview Cuticle Epidermis Veins  H20 Stomata  CO2 Mesophyll  Chloroplasts 5 Chloroplasts Stroma  CO2 reduction Grana Thylakoids  Thylakoid space  Thylakoid membrane  Chlorophyll  Solar energy absorption  Photosystems  Enzymes & machinery  ATP manufacture 6 Light and reducing power Light-dependent reactions  Split H2O  Release O2  Solar energy captured  Light energy used to Reduce NADP+  NADPH  Generate ATP from ADP through photophosphorylation   NADPH & ATP used in Calvin cycle Carbon fixation reactions  CO2 converted into organic matter  Different plants perform carbon fixation differently  C3  C4  CAM 7 H2O Light NADP+ ADP P Light Reactions Chloroplast i H2O Light NADP+ ADP P i Light Reactions ATP NADPH Chloroplast O2 CO2 H2O Light NADP+ ADP P i Light Reactions ATP NADPH Chloroplast O2 Calvin Cycle CO2 H2O Light NADP+ ADP P i Light Reactions Calvin Cycle ATP NADPH Chloroplast O2 [G3P] (sugar) Light biophysics Light waves in photons  Energy content inversely proportional to wavelength  Gamma rays = shortest wavelength = highest energy  Radio waves = longest wavelength = lowest energy Ultraviolet light  Higher energy than visible light  Can disrupt DNA Visible light  Photon absorption depends on  Wavelength  Chemistry of molecule it hits  Each molecule has characteristic absorption spectrum Photoelectric effect 12 Pigments Molecules that absorb visible light  Carotenoids  Absorb violet, blue, green Light Reflected light  Reflect yellow, orange, red  Chlorophyll  Absorb violet, blue, yellow, orange, and red  Reflect green  Chlorophyll a – main pigment  Chlorophyll b – accessory pigment Absorbed light Transmitted light Chloroplast 13 Photosystems Photosystem STROMA Light-harvesting Reaction-center complex complexes Primary electron acceptor Photon Consist of  Light-harvesting complex  Hundreds of accessory  Reaction center complex  One or more chlorophyll a molecules Energy of electrons is transferred through the light-harvesting complex to the reaction center complex Thylakoid membrane pigment molecules e– Transfer of energy Special pair of chlorophyll a molecules Pigment molecules THYLAKOID SPACE (INTERIOR OF THYLAKOID) 14 Photosystem organization At the reaction center complex, the energy from the light-harvesting complex is transferred to chlorophyll a  Excites chlorophyll electron  Excited electron transferred from chlorophyll a to electron acceptor  Water donates an electron to chlorophyll a to replace the excited electron 15 Light-dependent reactions Primary photoevent  Pigment captures photon  Pigment electron gets excited Charge separation  Energy transferred to reaction center complex  Energized electron  acceptor molecule Electron transport Redox reactions  NADP+ reduced   Pump H+ ions across membrane  Concentration gradient Chemiosmosis  H+ move back through ATP synthase  ATP is produced 16 Bacterial photosystem Single photosystem Photon is absorbed Electron moves along electron transport chain  Electron joins proton  hydrogen Electron is recycled to chlorophyll Cyclic photophosphorylation  Electron path is circular 17 Plant photosystems Two photosystems (I and II) Photosystem II (PSII)  Best at absorbing a wavelength of 680nm  The reaction-center chlorophyll a of PS II is called P680 Photosystem I (PSI)  Best at absorbing a wavelength of 700nm  The reaction-center chlorophyll a of PS I is called P700 18 Photosystem II Light-harvesting complex chlorophyll absorbs photon  Energy is passed among pigment molecules until it excites P680 P680 transfers high-energy electron to primary electron acceptor thus beginning an electron transport chain  H+ pumped across membrane  ATP produced through chemiosmosis  Electron eventually transferred to photosystem I reaction center complex P680 electron replaced by the splitting of water  Produces O2 19 Photosystem I Light-harvesting complex chlorophyll absorbs another photon  Energy is passed among pigment molecules until it excites P700 P700 transfers high-energy electron to primary electron acceptor thus beginning another electron transport chain  Final electron acceptor is NADP+  NADP+ reduced to NADPH Noncyclic photophosphorylation 20 e– ATP e– e– NADPH e– e– e– Mill makes ATP e– Photosystem II Photosystem I Comparing chemiosmosis Chloroplasts and mitochondria generate ATP by chemiosmosis, but use different sources of energy  Mitochondria transfer chemical energy from food to ATP  Chloroplasts transform light energy into the chemical energy of ATP Spatial organization of chemiosmosis differs between chloroplasts and mitochondria but also shows similarities  In mitochondria, protons are pumped to the intermembrane space and drive ATP synthesis as they diffuse back into the mitochondrial matrix  In chloroplasts, protons are pumped into the thylakoid space and drive ATP synthesis as they diffuse back into the stroma Mitochondrion Chloroplast MITOCHONDRION STRUCTURE CHLOROPLAST STRUCTURE H+ Intermembrane space Inner membrane Diffusion Electron transport chain Thylakoid space Thylakoid membrane ATP synthase Key Higher [H+] Lower [H+] Stroma Matrix ADP + P i H+ ATP Calvin cycle overview Occurs in the stroma Carbon enters the cycle as CO2 and leaves as a sugar named glyceraldehyde-3-phospate (G3P) For net synthesis of 1 G3P, the cycle must take place three times, fixing 3 molecules of CO2  2 G3P molecules required to make 1 glucose molecule The Calvin cycle has three phases:  Carbon fixation (catalyzed by RuBisCO)  Reduction  Regeneration of the CO2 acceptor (RuBP) Calvin cycle – carbon fixation Carboxylation  3 CO2 molecules enter the Calvin cycle separately  Each binds to RuBP (ribulose 1, 5-bisphosphate)  Uses the enzyme RuBisCO – ribulose bisphosphate carboxylase / oxygenase Resulting 6-C molecules each split into two 3-C molecules Input 3 (Entering one CO2 at a time) Phase 1: Carbon fixation Rubisco 3 P Short-lived intermediate P 3P Ribulose bisphosphate (RuBP) P 6 P 3-Phosphoglycerate 25 Calvin cycle – reduction Each 3-C molecule is phosphorylated by 2 ATP molecules Each 3-C molecule is reduced by 2 NADPH molecules Calvin Cycle  NADPH oxidized back to NADP+ 6 ATP 6 ADP 6 P P 1,3-Bisphosphoglycerate 6 NADPH 6 NADP+ 6 Pi Resulting molecule is G3P 6 P Glyceraldehyde-3-phosphate (G3P)  6 G3Ps produced for every 3 CO2  Only 1 leaves Calvin cycle 1 Output P G3P (a sugar) Glucose and other organic compounds Phase 2: Reduction 26 Calvin cycle – regeneration 6 G3Ps produced 1 leaves Calvin Cycle to make glucose and other organic compounds Other 5 are recycled 3P P Ribulose bisphosphate (RuBP) 3 ADP  Phosphorylated by 3 ATP  Final result = RuBP 3 Calvin Cycle ATP Phase 3: Regeneration of the CO2 acceptor 5 (RuBP) P G3P 6 P Glyceraldehyde-3-phosphate (G3P) Output 1 G3P (a sugar) P Glucose and other organic compounds Alternative mechanisms of carbon fixation Dehydration is a problem for plants, sometimes requiring trade-offs with other metabolic processes, especially photosynthesis On hot, dry days, plants close stomata, which conserves H2O but also limits photosynthesis The closing of stomata reduces access to CO2 and causes O2 to build up These conditions favor a seemingly wasteful process called photorespiration Photorespiration In most plants (C3 plants), initial fixation of CO2, via rubisco, forms a three-carbon compound In photorespiration, rubisco adds O2 instead of CO2 in the Calvin cycle Photorespiration consumes O2 and organic fuel and releases CO2 without producing ATP or sugar In many plants, photorespiration is a problem because on a hot, dry day it can drain as much as 50% of the carbon fixed by the Calvin cycle Photorespiration RuBisCO also catalyzes RuBP oxidation  Results in CO2 release  Decreased yields of photosynthesis  Photosynthesis > photorespiration In hotter climates  Stomata closed to conserve H2O  CO2 cannot enter leaf  Photorespiration > photosynthesis C3 plants 30 C4 Plants C4 plants minimize the cost of photorespiration by incorporating CO2 into four-carbon compounds in mesophyll cells This step requires the enzyme PEP carboxylase PEP carboxylase has a higher affinity for CO2 than rubisco does; it can fix CO2 even when CO2 concentrations are low These four-carbon compounds are exported to bundle-sheath cells, where they release CO2 that is then used in the Calvin cycle C4 leaf anatomy Mesophyll cell Mesophyll cell Photosynthetic cells of C4 plant leaf The C4 pathway CO2 PEP carboxylase Bundlesheath cell PEP (3C) Oxaloacetate (4C) Vein (vascular tissue) ADP Malate (4C) Stoma Bundlesheath cell ATP Pyruvate (3C) CO2 Calvin Cycle Sugar Vascular tissue CAM Plants Some plants, including succulents, use crassulacean acid metabolism (CAM) to fix carbon CAM plants open their stomata at night, incorporating CO2 into organic acids Stomata close during the day, and CO2 is released from organic acids and used in the Calvin cycle Sugarcane C4 Mesophyll cell Bundlesheath cell Organic acid Pineapple CO2 CO2 1 CO2 incorporated into four-carbon organic acids (carbon fixation) CO2 Calvin Cycle CAM Night Organic acid CO2 2 Organic acids release CO2 to Calvin cycle Day Calvin Cycle Sugar Sugar (a) Spatial separation of steps (b) Temporal separation of steps