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Exam 2 Material
Biol200
| Question | Answer |
|---|---|
| How do we make ATP? | ATP is made in mitochondria |
| ATP synthase | Enzyme 'squishes' ADP+Pi together. Energy comes from gradient as H+ move [high] to [low]. |
| How is the H+ gradient made? | Energy to push H+ against gradient comes high energy e-, e- cause conformational changes. Electrons e- lose energy (give up to molecules in chain) |
| Quinone | Lipid pumping electrons. |
| Principles of Metabolism | 1)Occurs in small steps 2)Each step has its OWN enzyme 3)For most steps delta G~0 4)Some steps are highly exergonic (delta G<<0) 5)The Law of Mass Action drives the processes. |
| Glycolysis (sugar break) | Occurs in cytoplasm. Net=2 ATP per glucose. Steps 1,3,10 are the only highly exergonic steps. |
| Substrate-level Phosphorylation | Creation of ATP by transfer of P from another molecule to ADP. Does not require H+ gradient! |
| "Electron carrier"-NAD+ | Nicotinamide adenine dinucleotide |
| Linking Step (in mitochondria) | Pyruvate, NAD+->NADH, HSCoA in, CO2 out, makes Acetyl CoA |
| Krebs Cycle | For each molecule of glucose: 2ATP, 6NADH, 2FADH2, 4CO2. |
| Lots of NADH and FADH2 So we have two problems... | 1) Get the energy from the electrons to make ATP: Electron transport chain -> H+ gradient ADP+Pi+energy->ATP(oxidative phosphorylation) 2)Get rid of low energy electrons 1/2 O2 + 2e- +2H+ -> H2O |
| The E.T.C is a series of redox reactions | Each reaction is delta G- In each case, the molecule that receives 2e- is a substrate for next rxn. |
| How much ATP is made? | NADH~2.4 ATP FADH2~1.4 ATP + 4 SLP ATP In eukaryotes grand total 29 ATP/glucose |
| Problem in Eukaryotes | NADH made in glycolysis is in cytoplasm. "NADH->FADH2" shuttle electrons from NADH through several proteins ultimately onto FAD in matrix |
| Prokaryotes:No mitochondria | ET/ATP synthase in plasma membrane. 31 ATP/glucose. NADH from glycolysis goes straight to ETC |
| Endosymbiont Hypothesis | Mitochondria have 2 membranes, mtDNA(circular)+ribosomes, mitochondria and bacteria are the same size, mito reproduce independently. |
| Other molecules can be used to make ATP! | Amino acids, pyruvate, coenzyme, fatty acid... |
| "Aerobic Organisms" | Use O2 as final e- acceptor. When O2 is low, all e-carriers are reduced. Pyruvate goes through alcoholic fermentation, gives off CO2. NADH oxidizes to make ethanol. |
| Anaerobic(no air) Organisms | LIve in low or zero O2 environment. ET chain use a different final e- acceptor. |
| Why would a cell regulate how much of each type of protein it has? | Save energy(not waste ATP), regulate responses to changes in cell to changes outside cell, save space, different cell types. |
| Molecules have a limited "lifespan" Why? | 1) Cells will destroy a protein if no longer needed. 2) Proteins get damaged radiation, oxidative damage. |
| Various Strategies for Regulating Protein Amount | A. Only transcribe when protein is needed "Regulation of Gene Expression" B. Degrade mRNA at a faster rate C. Regulate rate of translation D. Regulate degradation of protein |
| In Prokaryotes: Rate of Transcription is related to promoter sequence | "Consensus sequence" Best binding site for sigma |
| Constitutively Expressed Genes | Enzymes for respiration, tRNAs, rRNAs, RNA polymerase, Sigma |
| Regulated Genes | Only expressed at certain times, places, conditions. |
| Which gene is most likely to be regulated in its expression? | B. a gene that codes a protein that is expressed only in muscle cells. |
| Eukaryotic Gene Regulation | "enhancer" elements , TATA box, promoter proximal elements, basal T.F.'s, co-activators, regulatory T.F's bind to PPE and enhancers |
| "PRE" | progesterone response element, the binding site for a T.F. that is activated by progesterone |
| "GRE" | glucocorticoid response element, the binding site for a T.F. that is activated by cortisol |
| "cAMP" | cAMP response element, the binding site for a T.F. that is activated by cAMP |
| Splicing Occurs in the Nucleus | Proteins assemble to make a spiceosome. snRNA catalyzes the cutting and reformation of phosphodiester bonds (another ribozyme). Introns are degraded to nucleotides. |
| Topoisomerase | Cuts and reforms backbone to relieve tension |
| Errors lead to mutation | If not fixed, then at next DNA rep. Permanent base pair change. |
| DNA polymerases can proofread | 1)senses mismatch 2)cut out N.T's 3) remakes new strand |
| Types of mutations in protein coding genes | 1) Silent, no change 2) Missense or single A.A. change 3) Nonsense or early stop 4) Frameshift: insertion or deletion |
| Cell Cycle Regulation or "when do I divide?" | Accelerators/Proto-oncogenes ->G1 checkpoint/STOP tumor suppressors->S->G2 PO then TS |
| Checkpoint is time when cell decides to to divide | G1 checkpoint-cell determines enough space? resources? energy? G2 DNA correctly replicated are organelles ready? |
| Cancer | uncontrolled cell division |
| Metastasis | Cells break off a travel through body and start new tumors. Tumors disrupt organ function. Cells lose their normal function. |
| Sources of mutation | Genetics-inherited like random mistakes, Viral-some viruses insert DNA in protooncogenes to activate them, Carcinogens-radiation and chemical |
| Sex | Creates genetic variation in next generation. |
| Gametogenesis | Gamete making, 2N->meiosis 1N gamete |
| Fertilization | Making a zygote. 2x1N fuse together 2N zygote |
Created by:
c13luong
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