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Human Gene expression Expressing a gene RNA polymerase binds to promoter, p region, ONLY when effector binds to enhancer element region of DNA RNA polymerase adds nucleotides to growing RNA polymer according to base sequence in DNA sense strand. ee p gene __________________________________ ________________________________DNA_ p gene __________________________________ _________________________________ RNA RNA polymerase RNA STAND RNA polymerase DNA STRAND Compare codes and products OH 5’P end O RNA SYNTHESIS -decodes DNA O OH O OH growing O RNA strand DNA template O Master audio tape Gene/DNA Code is pattern of metal oxide on tape Code is sequence nucleotides. Cassette tape decodes Master. RNA decodes DNA. Product is sound. Product is protein OH RNA pol :O H enzyme O OH OH Decoding the Master tape (mRNA is decoded on ribosomes) Master tape DNA RNA cassette tape Tape player decodes cassette tape Code is transferred to cassette tape. Tape must be perfectly packaged to produce the product, Sound . Gene Expression Gene Expression Enzymes form RNA from sequence of nucleotides in tiny region of DNA, passing on the code to be decoded on the ribosomes. RNA polymerase adds nucleotides to growing RNA polymer according to base sequence in DNA sense strand. p gene __________________________________ _________________________________ RNA RNA polymerase Modification of mRNA mRNA mRNA tail cap cap tail cap (me G) and poly A tail are added to protect mRNA from cellular enzymes that would degrade it ribosome mRNA moves through ribosome M A mRNA M tRNA-adapter amino acid Decoding mRNA (translation) A peptide bond forms Translation of mRNA mRNA A M mRNA tail A M Translation of mRNA tRNAM leaves S mRNA is moving through ribosome as protein is forming Translation of mRNA mRNA G C mRNA V L V mRNA is moving throughribosome as protein forms S A G protein is formed C S M mRNA L STOP codon at end of mRNA halts protein formation stop codon protein is formed G C S S A A 1 M M A M 1 stop codon newly-made protein must be modified before it becomes active H V H H A M Modifications to newly-made proteins 1. Remove signal sequence (often at N-terminal end of protein) 2. Add acetyl group to new N-terminal Remove signal sequence met-ala-ser-cys-val-ile-tyr-phe-ala-pheNH3 Signal sequence directs newly-made protein to correct location in cell. 3. Add -OH groups to pro or lys Signal sequence is removed by proteases when protein reaches cellular destination. 4. Add glucose to asn or other a.a. units Add acetyl group to new N-terminal glycogen glu glu f-6-P ala-phe-his-glu-asn-gln-pro--------NH C=O CH3 - acetyl group prevents cellular proteases from degrading protein too rapidly Normal levels of blood glucose range from 90 - 110 mg / 100 ml. As glucose levels fall below 90 mg/dl, glucagon is secreted and binds to liver cells; glycogen is degraded and blood glucose levels rise. gly.P f-1,6-diP 3-PG OAA PEP malate malate Blood glucose levels g-6-P DHAP pyr pyr OAA gly.P pyr malate DHAP acetyl Co A citrate OAA succinate succ.CoA isocitrate G Pasteur Effect Glucose consumption and lactate formation decrease when cells use much more oxygen. Explain the molecular basis for this. in cells with low oxygen glycogen glu glu g-6-P glu g-6-P f-6-P f-6-P f-1,6-diP 3-PG OAA PEP cells with high oxygen glycogen glu DHAP gly.P NAD:H pyr lactate malate gly.P f-1,6-diP NAD:H 3-PG DHAP gly.P OAA PEP malate malate pyr pyr OAA pyr malate DHAP acetyl Co A citrate OAA succinate succ.CoA isocitrate G Molecular basis for Pasteur Effect Molecular basis for Pasteur Effect - when O::O usage increases, much more ATP is formed since TCA cycle and ETS operate - as cells increase use of O=O, cytoplasmic NAD+ is regenerated through -glycerol P shuttle - increased [ATP] inhibits pfk and rate of glycolysis decreases, lowering glucose consumption - thus the rate of lactate formation is decreased Oxygen debt When severe exercise ends, the increased rate of respiration (O=O consumption) continues for several minutes. Increased intake of O=O is required to accept electrons still in ETS. Energy requirements for marathons Approximately 100 Kcal/mile for 26 + miles are expended, regardless of the pace. - 2600 Kcal is required; more if temp. is over about 65°F Fuel reserves fuel tissue amt./ave. man* glucose blood 40 Kcal glycogen liver muscle 200 Kcal 400 Kcal triglycerides adipose 100,000 Kcal protein muscle 25,000 Kcal Use of fuels heart fatty acids used to form ATP for muscle contaction skeletal muscle fatty acids and some glucose used to form ATP for muscle contaction brain absolute requirement for glucose * ave. 155 lb. man Fuel Utilization in marathon possible actual fuel sources miles miles to depletion glucose in blood 0.5 2-3 glycogen liver 2.0 4.0 11 20 - 26 fatty acids many 26 +++ protein not available for energy muscle Skeletal muscle fibers % fiber type ave. Olympic Olympic quadriceps man sprinter marathoner Type I (aerobic) 58 30 80 Type II (anaerobic) 42 70 20 % fiber content is genetically determined . [glycogen] is same for both fiber types. Muscle fibers Skeletal muscles are composed of 2 types of fibers: Type I red fibers (aerobic,oxidative) -used for prolonged work Type II white (anaerobic) -used for high intensity work of short duration Endurance training 1. induces proliferation of mitochondria in Type I fibers 2. increases %Type IIa fibers (have some oxidative capacity) 3. increases capacity of body to mobilize fuels (fatty acids,glucose) by increasing vascular system Hormonal control of blood glucose - normal [ glucose ] in blood varies from 80 - 120 mg/100 ml - brain requires [ glucose] above 90 mg/100ml for maximal function Hormonal control of blood glucose Liver cells -glucagon binds to receptor protein in liver cell membrane resulting in increased cAMP formation, breakdown of glycogen and release of glucose into blood Glycogen depletion Fuels used blood glucose glucose from liver glycogen g-6-P from muscle glycogen fatty acids from fat cell trigly skeltal muscle glycogen depletion mile # 1-3? 3-18? 11-? 2-26+ exhaustion Hormonal control of blood glucose Skeletal muscle - insulin binds to skeletal muscle receptor protein causing increased cAMP formation and stimulation of glucose transport into muscle cells - decreases blood [glucose] dramatically Hormonal control of fuel reserves Adipose cells - glucagon binds to receptor protein in adipose cell membrane stimulating cAMP formation, accelerating breakdown of: triglycerides fatty acids + glycerol Glycogen loading - to do “glycogen loading”, the runner must deplete the glycogen stores by running 20 miles, several days before the event -then eating a diet high in CHO’s for several days replaces the glycogen and adds as much as 30% more