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Bio 141 Second half of semester

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by: Kainath Merchant

Bio 141 Second half of semester Bio142

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Kainath Merchant
Emory University
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These notes are brief, yet crucial things to remember for the second half of the semester in Bio 141.
Bio 142 - Abreu
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This 21 page Class Notes was uploaded by Kainath Merchant on Thursday January 14, 2016. The Class Notes belongs to Bio142 at Emory University taught by Abreu in Spring 2016. Since its upload, it has received 71 views. For similar materials see Bio 142 - Abreu in Biology at Emory University.

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Date Created: 01/14/16
Second part of Semester Monday October 5th Membrane transport Permeability? - High Permeability: small non polar molecules (O2, C02, N2) - Small, uncharged: (H20) Low permeability Large, uncharged polar molecules (glucose) - Ions: Cl-, K+, Na+ 4 Things influence bilayer Fluidity and Permeability 1. Fatty Acid Saturation (# of C-C, or C=C) 2. Fatty Acid Length (how many carbons/length of tail) more fluid with less kinks 3. Temperature 4. Cholesterol Content Fatty Acid Saturation is a function of C=C double bonds - unsaturated (kinky) or shorter fatty acids increase permeability MORE permeable with SHORTER fatty acids and MORE UNSATURATED longer it is, the more surface area it has interactions with Cholesterol LOWERS Bilayer permeability and fluidity Cholesteral (amphipathic, so polar head group) inceases density, —> decreases permeability and fluidity more density —> less permeable decrease temperature —> lower fluidity Increase phospholipids can move laterally throughout the lipid bilayer. They rarely flip between layers - Phospholipids are in constant lateral motion, rarely flip to the other side of bilayer - strong interactions between polar head groups and water, so stabilizing H bonds - unfavorable for polar molecule to go through hydrophobic core Rainbow trout:what changes occur within plasma membrane to permit a wide temperature range - Can change cholesterol—> affects fluidity - would have more unsaturation - fluidity increases as temperature decreases Why do molecules move across lipid bilayers? Diffusion: random movement of molecules from regions of high concentration to low diffusion is spontaneous (kinda like falling down a slide) low entropy/high order —> high entropy/low order spontaneous: PASSIVE transport Osmosis: diffusion of water, movement of water (same as diffusion but in water) 1. Osmosis only occurs across selectively permeable membrane 2. if there is a concentration gradient Water moves from low solute [ ] to high solute Tonicity in hypotonic solution: water comes into cell Fluid Mosaic Model plasma membrane more than just a bilayer Hypotonic: less solute , water goes into cell Hypertonic: more solute in cell, water goes out to equal concentration gradient Isotonic: equal solute, net direction equal Cells constantly move things in and out of cell to do their jobs Few things can get through lipid bilayer Cells can change proteins and locations to determine what gets in Three main transport mechanisms 1. Simple Diffusion 2. Facilitated Diffusion 1. via CARRIER protein 1. Substrate binding 2. Via CHANNEL protein: passageways to allow things to go down their gradient Protein Structure determines SPECIFICITY, 1. 3. Active transport via pumps (opposite of diffusion) (PUMPING in opposite direction of diffusion) **cells like a -potato chip —> salty (Na) on outside, potato (potassium K) inside 1. Passive transport: requires no energy, driven by concentrating gradient (like skiing downhill) Active transport: requires input of energy (like climbing mountain), proteins pump molecules 2. AGAINST their gradient Facilitated diffusion by transporters occurs down a concentrated gradient A glucose transporter, such as GLUT-1, increases membrane permeability to glucose - Ion channels are GATES that open/cloe based on a response - Once gate opens, movement is PASSIVE (no energy needed) - Two forces trying to reach equilibrium - membrane potential = separation of charges Cell like a battery: separates charges we are always fighting molecules trying to reach equilibrium to stay alive protein PUMPS molecules AGAINST their gradient - needs energy, very important in nerve cells Aquaporins, rapidly transporting water (channel that is always open - leak channel) go either way, depends on driving force on water - selective water channels - found in many cell types - tightly regulated - needed for maintaining osmolarity adding aquaporin —> increase osmosis—> increase permeability of water, maintains cell volume in hyper/hypotonic environments protein = function expression: - where? - how much? - when? 2 driving forces on ions: - concentration gradient - separation of charge on membrane (membrane potential) Why bold a concentration gradient in first place? - think of damming water, where lots potential energy used to drive other processes - can couple other reactions with diffusion, can drive ATP synthase molecules - can transfer things against gradient, etc. Cells All cells are ribosomal Eukaryotes: (bacteria + archaea—> closer to eukaryotes) - true nucleus - most are multicellular - can be single celled (yeast) Prokaryotes - thought to have evolved “before: - mostly unicellular (single cell) - domain was split in 19777 based on rRNA genes - archaea more closely related to Eukaryotes - do have cytosol, but not organelles biggest difference: Eukaryotes: nucleus All cells: - DNA - ribosomes (site of translation) - cytosol (mix of water and solute inside the cell) - membrane (defines barrier to exterior of cell) Differences: - size (eukaryotes much larger, eukaryotes > prokaryotes) - nucleus (euk have) - more cytoskeleton - membrane-bound organelles - organelles (compartments within cells with a unique function) Cytosol: mix of water and solute cytoplasm = cytosol + organelles organelle: membrane bound (except ribosome) structure with specific purpose. ribosomes: all cells, protein synthesis rough ER/smooth ER: eukaryotic lysosome: breakdown of macromolecules via hydrolysis “hydrolytic enzyme” vacuole: storage of water or anything the cell might need, where you will find pigments for color, and toxins specialized lysosomes in plans (same job in animal cells, vacuoles do in plant cells) peroxisome: breakdown via redox byproduct is hydrogen peroxide H202 —> free radicals, DNA damage Mitochondrian: found in all eukaryotic cells energy production 2nd half of cellular respiration, makes ATP Chloroplast (opposite of mitochondrian) only in plant cells, captures solar energy to convert to energy All cells: cytoskeleton more complex in eukaryotic cells plasma membrane cell walls Wednesday October 14th Endosymbiosis Theory: mitochondria and chloroplasts evolved from prokaryotes that were engulfed end: larger engulfing into smaller. symbio: benefit to maintain membrane bound organelle - can arise from pre-existing mitochondria and chloroplast - have their own genome - single circular chromosome similar to bacteria - mitochondrial inheritance from mother (ovum) - have their own protein synthesizing machinery (have own ribosomes, able to be blocked by antibiotics which dont affect cytoplasmic ribosomes) - Draw/describe location and function of major organelles…. look at learning objectives on lecture slides Friday October 16th How do molecules get across the membrane? diffusion (passive, facilitated, active) How do big molecules cross? - Endocytosis - Exocytosis - golgi —> vesicle—> cell membrane Endomembrane system composed of endoplasmic reticulum, the golgi apparatus, lysosomes primary system for protein and lipid metabolism smooth ER: 1. lipid metabolism (enzymes doing both synthesis and degradation) 2. Calcium storage Rough ER (covered in ribosomes, which are main for protein synthesis): protein synthesis metabolism: synthesis: anabolism (synthesis/building things) degradation: catabolism (breaking things apart) Small molecules diffuse randomly thought cell, but protein movement and large molecules diffusing throughout the cell, need a lot of energy and tightly regulated. Secretory pathway: proteins intended for secretion from the cell are synthesized and processed in set of steps Proteins are packaged into vesicles when move from the rough ER to the golgi apparatus molecular “Tags” ~ zipcode ~ street address ER signal sequence binds to a signal recognition particle SRPthat binds to a receptor in the ER membrane. Once inside rough ER, proteins then folded and glycosolated (glycosylation: carbs attached to the protein) golgi apparatus: further processing of proteins post translational modifications, like glycosylation protein trasnmitted by ribosome, deposited inside, then processed Proteins are transported from the ER to the golgi apparatus in vesicles that fuse with the golgi membrane and deposit their contents inside Golgi apparatus’composition is dynamic: new cisterna for at the cis face (protein entering rough ER) When proteins processed via glycosylation, oligosaccharides are added and modified - Protein products enter the gold apparatus at the cis face and pass through cistern containing enzymes for attaching specific carb chains - Each protein that comes out of golgi apparatus has a molecular tag that places it in a particular type of transport vesicle. 1. proteins are tagged 2. proteins are sorted 3. vesicles bud 4. proteins interact with receptors 5. delivery Proteins that go through sorting pathways 1. membrane bound organelles 2. integral membrane proteins 3. proteins that are secreted via exocytosis Integral plasma membrane proteins are highly glocysolated important for cell-cell recognition, communication, and adhesion Pancreas cells secrete glucagon (protein hormone that raises blood [glucose] glucose concentration) Protein synthesis and transport Ribosom site of translation cytosolic proteins secretory and membrane bound are tagged for the ER Endoplasmic Resticulum rough ER: studded with ribosomes smooth ER: lipid metabolism Lysosomes structure with single membrane containing 40 different digestive enzymes. found in animal cells How are materials delivered to lysosomes? 3 processes Autophagy Phagocytosis endocytosis is a process by which the cell membrane can pinch off a vesicle to bring outside material into the cell bring something via endocytsosi, then delivering to lysosome to be broken down Receptor-mediated endocystosis Endosome matures into a lysosome Hydrolysis: enzymes within the lysosome catalyze hydrolysis reactions to breakdown macromolecules Nucleus: - double membrane: nuclear envelops - info storage and processing - transcription happens here - nucleolus: where rRNAsynthesis happens Nuclear envelope: double membrane surrounding that defines the nucleus, each membrane has a lipid bilayer, continuous of endoplasmic reticulum. inner surface: continuous with fibrous proteins called nuclear lamina How are molecules imported into the nucleus? molecular tag mRNAand ribosomes are synthesized in the nucleus and exported to the cytoplasm. things like proteins are needed in the nucleus are then imported in the nucleus Monday October 19th Cytoskeleton Cytoskeleton: network of fibers that helps cell maintain its share by providing structural support Microtubules - intermediate - actin filaments cytoskeleton is dynamic, can alter the cell’s shape 3 types of protein filaments, differ from size, protein components, cellular location, and function. 1. Intermediate filaments: support/structure only cell specific, 10nm 2. microtubules: involved in movement and position of organelles , movement of chromosomes during cell division largest, 25nm, 3. Actin: cell motility (movement of entire cell, or movement f compartment of cell) 7nm 1. Actin filaments: smallest cytoskeletal elements, protein formed by polymerization of individual actin proteins free moleucles: bound toATP, catalyzes fromAtp toAdp, hydrolyzed toADP soon after actin is incorporated into a filament , becomes unbound weakATPase, but has ability to convert stuff fromATP toADP. (ATPase: can bindATP and throw off phosphate group) defines cell shape moves boundaries and borders of cell actin can be involved in movement by interacting with moto protein myosin a. actin and myosin interact to cause movement Sacromeres are the contractile units of muscle 2. Intermediate filaments: defined by size rather than composition - many types exist, but each has a different protein NOT involved in movement only involved in structural support for the cell intermediate filaments provide cells with mechanica strength 3. Microtubules: built from tubulin molecules, dimers of alpha and beta tubular proteins dimers stack together to form a hollow, cylindrical microtubule Microtubules act as “railroad tracks” to transport vesicles through cell in energy-dependent process motor proteins bind microtubules and use energy fromATP hydrolysis to move cell components along the filament (can call the motor proteinsATP-ases) Motor proteins, two families: kinesins move towards plus end of microtubules (anterograde direction) away from nucleus dyneins move towards mine end (retrograde) MTOC: microtubule organizing center (negative end towards mtoc) centrosome: located near the nucleus, gives us that directionality in animal cells, centrosome made up of two centrioles, always help organize directionality of microtubules should be able to tell which motor protein is lining up with which element Wednesday Oct. 21 Two types of cell division: meiosis and mitosis compare and contrast: Meiosis: leads to production of gametes (egg and sperm) - daughter cells have half the amount of genetic material as the parent cell - essential for sexual reproduction Mitosis leads to production of all other cell types (somatic cells) - genetic material is copied then divided equally - daughter cells are genetically identical to the parent cell, exact copy - responsible for three key events in multicellular eukaryotes: 1. growth 2. wound repair 3.asexual reproduction Eukaryotic chromosome contains single double helix of DNAwrapped around proteins genome: entire blueprints that make up organism gene: section of DNAthat hasALL info to make a specific protein or RNA Chromosome structure changes before and during Mitosis Each chromosome is replicated prior to mitosis Each of the DNAcopies in a replicated chromosome is a chromatid interphase —> mitosis —> cytokinesis —> interphase Why is it important to regulate cell growth could cause mutations, wrong type, too much, not enough Growing cells cycle between a dividing phase Cell cycle: orderly sequence of events that occurs from formation of eukaryotic cell through duplication of its chromosome to the time it undergoes cell division. gap phases: allow cells to grow First gap - G1, occurs before S phase S phase: chromosome replication Second gap - G2 Interphase G1 + S + G2 Mitosis - M phase Two sister chromatids Friday October 23 DNAreplication Genome: all of the genetic information that defines an organism, which includes all coding and non-coding things genes: coding genetic code: universal, therefore, similar DNAsequences yield proteins with same primary amino acids Structure = functions proteins with similar sequences will carry out similar functions Homology genomes that share a common evolutionary ancestor therefore similar sequence Subtle variations between individuals SNPs: single nucleotide polymorphisms Mutations: may be null or harmful or beneficial Review of DNAstructure a. structure of deoxyribonucleotide a. phosphate attached to 5’carbon of the sugar b. direction of DNApolymerization: 5’—> 3’ c. phosphodiester links Meselson - Stahl experiment 1. grew bacteria in some form of media 2. in that media, added different isotopes of nitrogen 1. parent generation: heavy isolate DNA, then separate by centrifugation (by spinning really fast) spinning can separate gradient of light, medium, and heavy types of DNAfor each generation 3 possible ways for DNAreplication: semiconservative —> parent DNAused as a template to make daughter copy to make identical. idea: middle would be unzipped hydrogen bonds so that daughter strands would have one strand from parent genome, and one strand from newly synthesized DNA conservative: next generation, parent DNAwould remain intact, then would have a brand new molecule of daughter DNA. nitrogenous bases would turn out to act as template. then replicate entire new daughter molecule parent: band at n15 gen1: have a band at each weight- n14 and n15. gen2: one would be n15, three would be n14 dispersive: short segments would be synthesized and then pieced back together parents bands in (heaviest) at N15 (isotope) as opposed to N14 Rules of replication: 1. DNAadds onto a 3’end 1. growns 5’—> 3’ 2. DNAcannot be added without an end, but RNAcan. therefore, DNAadded on to a short RNA(“primer”) 3. DNAis antiparallel therefore, leading and lagging strand of replication fork Monday October 26th End of M phase, beginning of G1 —> blob, decondensed G1—> synthesis of organelles, no change ins structure YET S1 —> change in structure, dna replication Describing a GENOME chromosome: separate units of DNAthat represent unique proportions of the genome sister chromatids: newly replicated copies, still attached at the centromere, spindle attaches to kinetochore proteins at centromere haploid number = number of unique portions of the genome or chromosomes ploidy: (#n): number of copies of each kind of chromosome, haploid: 1n, diploid: 2n, triploid: 3n one material copy + one paternal copy, humans are diploid Human genome: 23 different kinds of chromosomes (haploid #) 22 kinds of autosomes X or Y sex chromosomes diploid: 2 copies of each —> 46 chromosomes gametes are products of meiosis, where daughter cells contain 1/2 of the parent cell genome somatic cells are the product of mitosis, where daughter cells are identical to parent cells diploid because there are 2 copies of each polyploidy multiple copies of each chromosome triploid (3 copies of each chromosome) tetraploid (4 copies) hexaploid (6 copies of each) stages of mitosis: memorize the steps and how the cell looks **** know different kinds of enzymes and their functions Enzymes for DNAreplication 1. The helix is opened and stabilized Helicase enzyme breaks the hydrogen bonds between N-bases, unzips DNA SSBP’s bind to stabilize sing strands, help to stabilize single stranded units, prevents strands from just snapping back together topoisomerase: clips back of sugar-phosphate backbone and relieves replication tension/ relieves torque 2. DNAnucleotides are added onto the 3’end primase synthesizes the RNAprimer (short strand that serves as starting point for DNA synthesis) DNApolymerase synthesized DNAcomplementary to the parental template strand in the 5’to 3’direction Synthesis of leading strand towards the replication fork 3. Synthesis of the lagging strand away from the replication fork okazaki framents are stitched together by ligase enzyme ****practice drawing replication fork 3’ — > 5’ top: synthesis will be in 5’to 3’so on right, direction will go towards replication fork (leading — >) top left lagging <— bottom left: leading <—, bottom right: lagging —> replisome: all the proteins necessary to replicate the leading and lagging strands making two identical copies of the DNAgenome problems with synthesizing a large genome: continuous replication on leading s trans discontinuous: lagging **telomeres problems at telomeres: gap being left over, which would cause ends of DNAtog et shorter after each cell division telomerase (rna + primer) has bits of RNAprimer, binds at complementary repeat, synthesize new DNA(has space for new RNAto come in and fill in gap) which strand- leading or lagging- requires telomerase? Telomere length does not mean longevity telomeres are going to shorten over lifetime because enzyme telomerase is not active in most somatic cells Telomerase IS active in germ cells, which gives rise to gametes and somatic stem cells telomerase is active in most cancer cells Mutation = a change in DNAsequence Human diseases: Mutation = cancer Repair: XP and HNPCC 2 diseases due to repair defects: - XP - HNPCC both genetic, so found in gamete cells A. causes of mutations 1. spontaneous, ex- polymerase error 1. due to replication errors, like substitutions, insertions, deletions) 2. replication errors: 1. prevention of proofreading 2. repair of replication errors by Mismatch repair (MMR): recognizes mistake, cuts it out, tries again HNPCC: hereditary non-polyposis colon cancer - defect in MMR genes, so no repair - errors remain - leads to cancer 2. induced, ex = UV irradiation 1. repair by photo reactivation or excision repair 2. UV radiation causes pyrimidine dimer, kink in DNA, blocks transcription (DNAdoes not like uv radiation) pyramidine dimer: two thymine next to each other, now have a covalent bond between each other —> causes DNAto kink outward. XP —> increased sensitivity to UV due to defect in excision repair (dont have nucleotide excision repair) nucleotide excision repair = specifically recognizes thymine dimers 1. enzymes detect irregularity in DNA 2. cut out DNAthat is damaged 3. DNApolymerase fills in the gaps in the backbone (where ligase comes in and glues up together) reversal (photoreactivation) enzyme called photolyse that reverses photodimer B. types of mutations 1. consider location - what kind of cell type it will be in 1. somatic and germ cells 1. somatic —> think of body as mosaic, many different cell types. can have mutation in just one cell type (skin cells —> skin cancer) 1. specific to cell type, specific type of cancer 2. germ line —> passed on to offspring 1. inherited phenotypes 2. genetic diseases 2. molecular change- base substitution? insertion? deletion? 1. insertion/deletion/rearrangements 2. base substitution - could be transitions (purine switching to purine, change ofA(purine) to G (purine)) or transversions ( purine switching to pyrimidine) C. Effects 1. effect on protein expression The genetic code is a. universal, code = same protein in all organisms b. redundant (most amino acids have more than one codon) C. UNAMBIGUOUS, every codon will only give you one amino acid d. Non-overlapping, Ribosome always reads “in frame” once translation begins how many reading frame are possible if we didn't have the universal start codon? **UNIVERSAL START CODON: AUG 3 possible reading frames, but the start codon e. Conservative: first two positions usually the same when multiple codons for amino acids. Alterations in translation, 4 possibilities: 1. silent mutation (change in nucleotide sequence, but doesn't affect primary amino acid sequence) 2. missense: change in nucleotide sequence, DOES give change in amino acid sequence 3. nonense: early stop codon, gives protein that is shorter than it should be, translation stops too soon 4. frameshift: insertion or deletion of a single base pair/nucleotide, now everything down stream is out of frame 5. sickle cell mutation: missions mutation because it is a single amino acid change (glutamate changes to valine, causes change in protein structure) effects on protein function: 1. neutral or conservative (no change in function of protein) 2. Null : doesn't work 3. hypomorphic (less function) 4. hypermorphic (increase in function) 5. conditional (function depends on conditions) 6. gain function or geomorphic Monday November 2nd Cell cycle checkpoints allow cells to divide only when they are healthy and in the right environment - enough nutrients - damage to DNA- repair - chromatids attached to spindle microtubules before cell enters anaphase - chromosomes have been replicated and DNAnot damaged - organelle production M phase checkpoints: 1. make sure chromosomes have attached to spindle apparatus 2. chromosomes have properly segregated and MPF is absent G1 checkpoints: 1. passes if cell size is adequate 2. nutrients sufficient 3. social signals are present 4. DNAundamaged, impaired correctly G2 checkpoints: 1. chromosomes have replicated successfully 2. DNAis undamaged 3. activated MPF is present What is MPF? there is “something” in cytoplasm that triggers the cell into M phase. what is it? experiment: took out cytoplasm from m phase cell, interjected into a cell that was in interphase, and yet it didn't enter m phase. so what is it? that “something: Called MPF: maturation promoting factor MPF is cyclin-cdk protein complex M-Cdk is a kinase (Cdk: cyclin dependent kinase) M-cyclin is a protein that regulates M-Cdk activity M-Cdk is ON when M-cyclin binds it kinase is enzyme that does phosphorylation (adds phosphate group to protein) phosphatase: removes phosphate group cyclin drops after M-phase, concentration decreases during interphase, increases again during m- phase (mitosis) M-cyclin is destroyed when Mitosis (M-phase) ends ubiquitin —> binds onto proteins and destroys the M-cyclin when protein no longer needed, tagged with ubiquitin to destroy to destroy small things, proteosome for degradation when Cdk and cyclin bind together, triggers phosphorylation effect when ready to go onto the next cell stage cycle, dephosphorylation comes in and inactivates the site, so now becomes active and can phosphorylate other proteins Cell cycle checkpoints> - is the cell’s environment ok? Rb protein is the switch, checks is cell environment is ok G1 checkpoints: Social control: Rb protein normally Rb is OFF and represses transcription Social signal (cell to cell communication): Rb protein 1. growth factor (mitogen) binds to receptor 2. activates Cylin-Cdk 3. Rb is phosphorylated when phosphorylated, Rb becomes inactive and releases regulatory protein and allows cell to proceed in cycle Tumor suppressor: p53 1. DNAdamage turns on kinase 2. kinase phosphorylates p53 3. p53 becomes stable and is not destroyed 1. more stable if phosphorylated and works against DNAdamage p53 binds to DNAand turns on transcription of another gene that turns on p21, which is a Cdk- cyclin inhibitor (which prevents replication of damage DNAand prevents from going into S phase) Cell cycle stops —> programmed cell death: apoptosis p53 is a DNAbinding protein, binds on regulatory proteins to turn on transcription both Rb and p53 are tumor suppressing genes like driving a car: proteins like those ^ put on the breaks if mutation on those genes, now you have a car with no breaks, and infinite replications ***Hallmarks of Cancer: 1. limitless replication potential (no more breaks/checks or balances, cell will grow without limits) 2. Evading apoptosis (avoiding programmed death) 1. apoptosis: cell death or cell suicide, eliminates cells without causing harm to other cells 1. gives us the correct number of cells 2. necrosis: cell just explodes signaling molecules tell cells what to do - survival factors: promote survival (suppress apoptosis) - M-phase promoting factors (stimulate division) - Growth Factors (stimulate growth of cell) Skipped Monday Notes Wednesday November 11th Catabolism: energy yielding metabolism Monday November 16 respiration is like controlled explosions energy of activation barrier overcome by enzymes ATP is like coins, energy = currency glucose are large bills in wallet fats and stored carbs are savings NADH and FADH2 are credit energy is released whenATP is hydrolyzed structures in/out glycolysis: glucose in —> pyruvate out pyruvate —> acetyl CoA oxalacetate —> citrate 2 main enzymes: know regulation of PFK and PDH know where the different steps are happening in the cell and in regards to eukaroyotes. steps of cellular respiration: 1. glycolysis takes place in cytosol glucose broken down into pyruvate 2. pyruvate processing pyruvate oxidized to form acetyl CoA 3. CitricAcid Cycle (also known as KREB cycle) Acetyl CoAis oxidized to CO2 (waste product) 4. Electron transport and chemiosmosis compounds reduced in steps 1-3 are oxidized in reactions leading toATP production glycolysis in cytosol - universal, every single cell can carry out glycolysis - 1. energy investment. put in molecule ofATP, which increases potential energy in substrates - only know what goes in and comes out, so phosphofructokinase. it’s a kinase, so phosphorylates a phosphorfructose. glucose gets phosphorylated glucose 6 phosphate gets rearranged into fructose 6 phosphate, kinase adds another phosphate group invest moreATP now split glucose into 2 three-carbon sugars went from 6 carbon sugar —> 2 three-carbon sugars, catalyzed by phosphofructokinase get out: 2 G3P’s PFK regulated byATP on phosphofructokinase, there are 2 binding sites forATP what kind of regulation?: allosteric regulation if there are 2ATP binding sites, how are they different? - cofactoring necessary for enzyme. active site: with high affinityATP is kinase substrate regulatory site: low affinity,ATP binds at high concentrations to inhibit PFk enzyme will be inhibited when lots ofATPis around fructose 6 phosphate is a substrate for phosphofructokinase. that kinase is phosphorylating a substrate, so needs a phosphate group from somewhere. where is that phosphate group coming from?ATP. one molecule ofATP is inhibiting the enzyme, but on the other site, it’s enabling to carry out functions feedback inhibition occurs when an enzyme in pathway is inhibited by the product of the pathway glycolysis: part 2 energy payoff 1. reduction: both molecules of G3P —> reduction: electron carrier is reduced —>ADP + phosphate = ATP G3P ends up becoming pyruvate, which is a 3 C sugar molecule 2 methods of producingATP (know when happen and what steps) 1. substrate level phosphorylation 1. occurs when: 1. ATP is produced by the enzyme-catalyzed transfer of a phosphate group from an intermediate substrate toADP ATP production: substrate level phosphorylation. needs an enzyme and a phosphorylated substrate IN: 1 glucose, 2ATP, OUT: 4 molecules ofATP (so net: 2ATP), 2 NADH, 2 Pyruvate transport to mitochondria cytosol —> mitochondria pyruvate processing and Kreb’s cycle within mitochondrial matrix, inside cistern need oxygen (aerobic) in order for cellular respiration to continue completely transferrin PE from pyruvate, completely oxidizing CARbons in form of pyruvate, yields HIGHATP yield. But anaerobic condition: fermentation can proceed even when there’s no oxygen. now pyruvate goes through incomplete oxidation, so not as muchATP incomplete oxidation —> FewATP ATP netted in fermentation, allows glycolysis to continue if there’s pxygen, pyruvate can go through 1. cellular respiration (goes into mitochondria) 2. if no oxygen, remains in cytosol, goes through fermentation, allows glycolysis to proceed Wednesday Nov. 18th Pyruvate still has potential energy most potential energy in non polar group, so CH3 is most non polar, where has the most potential energy Pyruvate (3 Carbon) goes to acetyl CoA(2 carbons) PDH: Pyruvate DeHydrogenase, inside mitochondria mitochondria: membrane bound with 2 membrane layers: inner and outer inside compartment referred to as mitochondrial matrix Enzyme PDH is occurring inside mitochondrial matrix Positive and Negative Regulation of PDH large multi enzyme complex located in the mitochondrial matrix PDH is positively and negatively regulated high concentrations of substrate speed up the pyruvate processing -AMP, CoA, NAD+, Pyruvate high concentrations of products inhibit via phosphorylation -ATP, acetyl, CoA, NADH Inhibition via phosphorylation. Enzyme called kinase, pyruvate dehydrogenate kinase, PDH kinase. inhibits PDH inhibit: substrates likeAMP, CoA, NAD+, Pyruvate (have a binding site on kinase) potentiate: products like :ATP,Acetyl CoA, NADH Acetyl CoAfeeds into Krebs Cycle (also known as citric acid cycle) Krebs cycle oxidize the crap out of citrate carboxylic acids that are oxidized during the cellular respiration **acetyl cos joins with ___ 2 C are released as CO2 for each acetyl K group. generatingATP by taking off pyruvate —> acetyl Coa, joins kern cycle …. LECTURE PODCAST 6 C glucose —> 6CO2 waste pyruvate and krebs takes place inside mitochondrial matrix first way of making atp: substrate level phosphorylation krebs cycle called a cycle bc: 4 carbona cid that accepts 2 carbons from acetyl CoAis regenerated it takes more energy to reduce NAD+ to NADH than to produceATP by substrate level phosphorylation - T/F *NADH takes more energy substrate level phosphorylation? change in energy is negative because exothermic Final step of cellular respiration: oxidative phosphorylation


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