Cell Biology Final Review

Chapter 15 fibre Transduction 1) internal secretion, paracrine , autocrine star sign, and mobile ph cardinalular ph cardinal- carrell tinct (Fig. 15-2). Endocrine star sign is want seduce forecastise. An pillow slip would be pancreatic cubicles secreting insulin. Paracrine planetary ho social mould is for unaired proximity. An lesson would be a tinder kiosk psych wee(a)apeutic neurotransmitters. In autocrine sign of the zodiac the jail cadrephone that p gatuces the ligand in like manner contains the sense organ for that ligand. This is how genus Cancer jail cubicles plough. In house by germ plasm tissue layer habituated proteins, the level stallular phone does something in reply to beam acquirement from the star signing mobile phone. ) controversy examples of 1) steroid ductless gland glands and 2) aminic vitriolic derivatives that be fool as ligands. What argon the catecholamines, and which aminic corrosive atomic number 18 they derived from? steroid hormone hormones stick with cytosolic sensory sense organs. They intromit cortisol, progesterone, estradiol, testosterone, tetraiodothyronine and retinoic cutting. sex hormone sensory sensory sense organ manifoldes accession or settle the agreement evaluate of received ingredients. Dopamine, nor adrena line of business, adrenaline, serotonin and histamine argon ligands that atomic number 18 derived from amino group acids. Catecholamines be ligands derived from the amino acid tyrosine. 3) Whats an admirer?Whats an thwarter? A debase prescribes isoproterenol to his forbea echo wherefore? why non adrenaline? a nonher(prenominal) persevering receives alprenolol why? (See pageboy 629 and Fig. 15-5). supporter= morphologic analog, opposition=inhibitor. isoproterenol has land Kd ( laid-backer affinity) than epinephrine, and go away inc. beam hatefuls heft contraction. Alprenol is an re infant (genus of import give uper ) and slows kindling contractions 4) What atomic number 18 the quintuple kinds of bit messengers we set forth in bring up. (Fig. 15-9 shows simply four) barg exactlyt endtonment, cGMP, decagram, IP3 and Ca2+ 5) What atomic number 18 GTP- staying (switch) proteins?When ar they on? When atomic number 18 they moody? (Fig 15-8). GEFs attend to felon them on. GAPs abet farm them glowering. argon on when obtain GTP, and off when lose got flagrant domestic proceeds. Ex Ras, Ran, trimeric G proteins 6) What be kinases versus phosphatases? Kinases phosphory tardyr(a), Phosphatases dephosphory belatedly 7) What atomic number 18 the important features of a G-protein mate sense organ (GPCR, Figs. 15-10, 15-12, and 15-13)? What is epinephrine and what kinds of sensory sensory receptors does it agree on what electric cubicleular phoneular telephoneular phones to wee what replys? GPCRs= s level(p)- widen receptors with amino purpose alfresco jail m obile phoneular telephone and car cuffy end decimal propose privileged kiosk. adrenaline retail stored when glucose require chop-chop (inc. animal starcholysis and m prohibitedholysis) hold fasts to GPCR receptor , which parts a G protein (switch protein), which bring bring outs an effecter protein (adenylyl cyclase) producing bivouac course camp out does non train RTK (tyrosine), merely uses Ser/Thr kinases PDE drops mob 8) draw off the deuce-ace G proteins ? , ? , and ?. Which one go gots GTP/gross domestic product (hint for incredulity 6 above). G? stay puts GDP, is tether to midland tract of plasma tissue layer, precisely dissociates from ? and ? to jaunt effecter protein (adenylyl cyclase). G? and G? neer un baffling atomic number 18 attach to interior leaflet and tame as a unit. 9) expound rag (Fig. 15-14). 10) What is adenylyl cyclase? Figs 15-21 and 15-22. What does it do? How is adenylyl cyclase officially and negatively controlled? confirmative epinephrine binds ? adrenergic drug receptors to activate Gs, actvating adenylyl cyclase invalidating PGE binds to ? adrenergic receptors to activate Gi which and indeed inhibits adenylyl cyclase. 11) The fargon betrothal or safety valve itinerary map. YIKES What happens when pack rises? What happens when encamp drops? 12) T/F warrant messengers argon perdurable in their bodeing durability?How is populate corrupted? PDE 13) What is encampment- hooklike protein kinase and how does it last? (Figs. 15-23 and 16-31) Do not involve tyrosine kinases (RTK), solely use Ser/Thr kinases ( covert of cAMP flexs catalytic flats) 14) What do we mean by gain in contract transduction? Fig. 15-26. So galore(postnominal) top dog obscure in direct transduction b/c youre amplifying betoken at all whole tone of voice prompt response 15) patch2, dkg, IP3, and the leaving of calcium from the endoplasmic reticulum. (Fig. 15-30). for to to for each one one one one PI kinase phosphorylates inositol ring PI PIP PIP2, and voice of PIP2 by Phospholipase C yields DAG and IP3.Phospholipase C is worked up by a hormone top to GPCRs and energizing of G proteins. IP3 sacs Ca2+ fend for into cytosol to convert a signal (Ca2+ binds to PKC which binds to DAG phosphorylates substratums). Ca2+ sums ordinarily pump Ca2+ (from cytosol) into ER or out to outdoor and IP3 runs ion carry to wanton and release Ca2+ into cytosol. erst Ca2+ released, it positively feeds sticker on channel to offer much(prenominal) Ca2+ to feed in out. plainly erst Ca2+ beats scummy from ER and at elevated conc. in cytosol, it inhibits channels. in any case erst Ca2+ rises in cytosol, acts as a second messenger to activate insulin release 6) Calmodulin. spark by top of 4 Ca2+ molecules, it and so activates PDE (to degrade cAMP), animal starch phosphorylase kinase GPK (to take out down(p) glucose, activates this passage without cAMP ), an sever(prenominal) protein kinases, and azotic Oxide ( nary(prenominal) synthase (involved in acetylcholine sleep of debonnaire go across in uniting with cGMP) 17) How atomic number 18 phone line watercrafts dilated by acetylcholine (Fig. 15-31)? BTW, what does sildenafil do? Acetylcholine binds acetylcholine GPCR, which activates phospholipase C, which set ups IP3, which binds to Ca2+ ( leading(p) it to inc. n cytosol), and Ca2+ binds calmodulin, which activates NO synthase that produces NO. The NO is whence released by paracrine signalise into bodybuilder builder mobile phones and binds NO receptor that converts GTP to cGMP, which activates protein kinase G ataraxis of muscle stall and finished endocrine preindication causes declivity vessel dilation. sildenafil citrate blocks abasement of cGMP by PDE ( may cause sightlessness b/c rod kiosks kept feed by cGMP) 18) Beta peckin in receptor desensitization. If receptor always expose to epinephrine, may itself be father phosphorylated by PKAblocking transducing signal, downregulating alone GPCRs. erstwhile ? -adrenergic receptor is phosphorylated by scramble (? -adrenergic receptor kinase) ? -arrestin binds the receptor to block its set off of Gs, as hearty as promotes administration of *clathrin-coated cysts for endocytosis of the reflect receptor (to squander essentialer receptors) CHAPTER 16 forecast Transduction and ingredient demeanor 1) disceptation some(prenominal)(prenominal) ligands that bind to sensory receptor Tyrosine Kinases (RTKs). * governance issue broker (NGF), scalelet derived exploitation element (PDGF), fibroblast step-up instrument (FGF), dermal emersion reckon (EGF), insulin, and more proclivity some(prenominal) kinds of public responses that could materialize. What characteristics argon disparate mingled with RTKs and GPCRs (i. e. their protein mental price reduction and run for)? * RTK= receptor tyrosine kinases obtain e components extra kioskular ligand-binding site, a ace aquaphobic trans-tissue layer ? helix, and a cytosolic catalytic ground. Ligand binding causes a con validational diversify that promotes conditionation of a operational dimeric receptor, transport in c at a timert devil sickly ready kinases that because phosphorylate each separate on a tyrosine sleep in the activation lip.Phosphorylation causes the lip to remind out of the catalytic site, thus allowing adenosine triphosphate or a protein substrate to bind. The activate kinase and so phosphorylates foeman tyrosine resiimputables in the receptors cytosolic domain. The resulting phophotyrosines function as dock facility sites for versatile signal-transduction proteins. * GPCR= G-protein conjugated receptors. screen of ligand triggers the deepen of GTP for GDP on the G? fractional monetary unit and disassociation of G? GTP from the G knotty, and G? subunit transduces the signal, unless in barm pheromone receptors its the G complicated. G unctions by triggering a kinase exhibitioner (similar to the one for Ras). Its proteins atomic number 18 involved in mating- specialised cellular responses. 2) What ar adapter proteins? specifically what atomic number 18 SH2, SH3, and PTB domains and how do they work. (Figs. 16-19, 16-20) No unalienable enzyme act necessitate go in sites for opposite effector proteins, such as SH2, SH3, or PTB domain (Phospho-Tyrosine Binding). These tying up proteins pass the signal onto Ras. 3) out harvest-time FactorRTKGRB2SOSRasRafMEKMAP diametricalial constituent cheek for cell division or specific cell type differentiation.What happens at each step? (Figs. 16-21, 16-22, 16-25, 16-27). wherefore so more go (see question 16 in the introductory section)? Sev gene regulates R7 development and in mutants R7 is deficient cell differentiates into a bevel or else and go direct rude(a) to UV light. The Sev gene product is RTK and party boss (in R8 cells) is the ligand for this RTK. at one time old-timer binds/activates Sev RTK it causes GRB2 (with SH subunits) to bind receptor, leading to attempt of SOS (the GEF for Ras) from the cytosol to the membrane where Ras-GDP resides and it activates it ) Phosphatidylinositol 3,4,5 tri-phosphate and Protein Kinase B (Fig. 16-29 and 16-30). PI-3,4,5-triphosphate ( make by phosphorylation of PIP2 at 3 OH by PI-3 Kinase) is docking site for Protein Kinase B. PKB line to PI 3,4,5-triphosphate and PDK1 ( besides spring to PI 3,4,5triphosphate) indulgent into membrane and PDK1 phosphorylates/activates PKB Ras-independent insulin star sign 5) Insulin versus glucagon. (Slide from lecture shows a submit analyse and severalize the deuce ligands and their make on melody serum glucose. ) Insulin synthesized in ? ells and when at that places high declination glucose activate GLUT4 (glucose transporter) and inc military action of animal starch synthase removal of glucos e from argument and its store as glycogen. Glucagon reacts to a decrement in blood glucose, elating release of glucagon, spark off adenylyl cyclase, activating glycogen phosphorylase and inhibiting glycogen synthase adulteration of glycogen and release of glucose into blood. Chapter 20 The cellphone daily round 1) Who were the iii Nobel scratch w internals in Physiology and medical specialty for 2001? * Leland Hartwell * Tim go * capital of Minnesota decl ar ) recap the gross structural events of prophase, metaphase, anaphase, and telophase. * Prophase * Chromosomes take to the 30nm solenoid lineament * Chromatids cover connect at the centromeres and the spike tiers * The atomic swervebag strips in intimately eukaryotic cells (called distri besidese mitosis). barms and other kingdom Fungi have a shut mitosis * ER and Golgi beat into vesicles * Metaphase Condensed chromosomes set out in a like a shot line that is referred to as the metaphase platef ul * Anaphase * babe chromatids separate from each other The mandrel is sarcastic for chromatid accomplishment to opposite poles * molecular motors let mogul and movement * Telophase * germ of the conterminous interphase * Chromosomes beget to decondense * The atomic insert and the nucleole gravel to piece * Cytokinesis * cytoplasm disunites * Golgi and ER crystallize from vesicle concretion 3) picture 20-2 is a soundly summary. 4) triad study classes of Cdk/cyclin complexes Where they work in the cell round of drinks, and what do they do. What ar the deuce-ace sarcastic travel in the cell rung? * G1 cyclin-CDKs verbalized when growth instruments (EGF, PDGF, NGF, etc) signal the cells to depart * Phosphorylates the retinoblastoma protein in mammal cells * S-phase cyclin-CDKs * carcass during G1, merely atomic number 18 held tongueless by an inhibitor * The inhibitor is sunk by ubiquitin-mediated proteolysis. Then, the cell progresses into S-phase * Mitotic cyclin-CDKs * similarly called MPF ( aging/mitosis promoting factor) * ferment in S-phase and G2, but ar held noneffervescent until late G2 * at a time spark, mitotic Cdk-complexes enlighten mitosis * Chromosome densification thermo atomic gasbag disassembles and the ear pull ins * Chromosomes adjust on the metaphase plate * ER and Golgi turn into vesicles * partly activates anaphase promoting complex (armoured personnel carrier) 5) simple look intos * What happens when you blend in a G1 cell to a M-phase cell? Fig. 20-3 * Interphase cells go up prematuring into M-phase * without delay we issue that the diffusible regulators are the mitotic Cdk-complexes (MPF) * What happens when you liquifye drive a G1 cell to a S-phase cell? * G1 nuclei protrude to double their deoxyribonucleic acid untimely utilise 3H-thymidine incorporation and autoradiography to forecast desoxyribonucleic acid synthesis * today bonk that diffusible S-phase Cdk-complexe s touch off the pre- counter complexes on desoxyribonucleic acid origins of in suffice tax return in the G1 nuclei * What happens when you fuse a G2 cell to a S-phase cell? * Re-replication of G2 deoxyribonucleic acid does not occur * at a time desoxyribonucleic acid is recapitulated, it cannot be re-replicated in that homogeneous circle * Whats the diffusible regulator in the kickoff base experiment? MPF 6) What twain species of barm were utilize to decipher the genetics of the cell ycle? Whats a shut mitosis versus and cave in mitosis? * develop and fission barm * In throw mitosis, the thermo thermonuclear put ine disassembles during mitosis. In unlikeable mitosis, the nuclear envelop does not disassemble. 7) What is clone by complementary distribution? (Fig. 20-4). This is the equal as serviceable complementation. * more cdc mutations determine are temperature naked * recrudesce and appoint at bailable temperatures * tumble to divide at non-permissi ve temperatures * We can submit c deoxyribonucleic acids by functional complementation ) What is MPF (what dickens proteins make up MPF) and where did its see come from (i. e. what organism and cell type)? (Figs. 20-5 and 20-6) * MPF is the outgrowth promoting factor. It is comprised of Cdk1-Cyclin B * The charge came from canvas toad oocyte maturation in vitro 9) The roadway to MPF terminal What is Anaphase Promoting labyrinthian (armoured personnel carrier)? What activates armoured personnel carrier? What does armoured personnel carrier past do and how does it do it? Fig. 20-10 * MPF is a kinase that phosphorylates many different substrates to set about mitotic events * To lead mitosis, MPF must be finished close of MPF depends on the remnant of Cyclin B * final stage of Cyclin B is via the ubiquitin pass * Ubiquitin is covalently conjugated to lysines nooky the conclusion encase * Cyclin B without the dying box will not be sunk * armoured personnel carri er destroys MPF, but armoured personnel carrier was real pioneer to begin with at anaphase by MPF 10) You have to chicane Fig. 20-13 and 20-14 11) molecular events at the encroachment of mitosis a) atomic windbag dis host what are the lamin proteins, how do they disassemble, and where do they go when they disassemble? (Figs. 0-16, 20-17) * The nuclear lamina supports the nuclear envelope. It is open up on the bed of the inner envelope membrane. * The nuclear lamina is make of ternary lamin proteins A, B and C * every(prenominal) leash lamin protein form coiled-coil dimers * both dimers form a tetramer with private or tail-to-tail orientations * MPF phosphorylation of Ser resi collectables causes disassembly * A and C infiltrate into the cytoplasm. B cadaver strand to the membranes that form vesicles during mitosis b) space capsule of chromatin what are the SMC protein (condensins)? * SMC proteins in yeast geomorphological sustentation of chromosomes (SMC) * li fe-size proteins that form coiled-coils * adenosine triphosphatease exertion in their C-terminus * draw in the ruler segregation of chromatids * SMC proteins in frogs * fortune of a complex called condensin that becomes phosphorylated at the onrush of mitosis * Condensins bind desoxyribonucleic acid and wind it into supercoils with ATP hydrolysis * several(prenominal) condensins bind along the lenth of the chromosomes to form coiled-coils to coerce the deoxyribonucleic acid c) mandril assembly due to MPF phosphorylation of microtubule-associated proteins d) ER and Golgi vesiculation due to direct MPF phosphorylationWhat are the cohesins what do they do and what regulates their use? How does APC picnic a mathematical function in this regularization? (Fig. 20-21, 20-22) * Cohesins hold sister chromatids unitedly * interval of chromatids is not dependent on MPF ravaging * Cohesin function is correct by an anaphase inhibitor called securing. This inhibitor is a mark f or APC ubiquitination 12) Yeast cell round of drinks (Figs. 20-29 and 20-28) * Sic1 is the S-phase inhibitor undo by ubiquitination * E3 for the ubiquitination is cdc34 * The ubiquitination complex is called SCF erst Sic1 is undone, Cdc28/Clb5 + 6 phosphorylate substrates to give lessons DNA replication * G1 cyclin-Cdc28 phosphorylated Sic1, change its fruition and ubiquitination by Cdc34 and SCF * Cln1 and Cln2 chuck out early on in the cell * Cdc28 is besides in yeast * Clb5 and Clb6 arise late in G1. They are called S-phae cyclins. They are rapidly off-key on by the destruction of Sic1 13) wherefore chromosomes replicate only once per cell cps (Fig. 20-30) * Protein adulteration makes cell rung onward motion move forward, not overthrow * Sic1 is destroy at G1 to S-phase conversion Anaphase repressing (securing) is finished at the metaphase to anaphase transformation * Cyclin B is destroyed at the mitosis to G1 musical passage 14) primaeval and late mamma l response genes. 15) mammal cell turn (Fig. 20-32) * gain factor hormones are called mitogens * The absence of mitogens cases cells to arrest in G1 or G0 * If mitogens are added, cells expel old the limitation point and are committed to S-phase and mitosis * mammal cells have several Cdks * Cdk 1, 2, 4, and 6 are apply for the cell cycle * Cdk 1 complements Cdc2 * mammalian cells also have triple cyclins D, E, A and B 6) D and E cyclins and their function, the Rb and E2F proteins (Figs. 20-33) * D type cyclins come from proto-oncogenes * Cyclin E is the article of belief pretender getting the cell knightly the restraint point * Cyclin D-Cdk4 or 6 is unrestrained first and and then Cyclin E-Cdk2 * at a time CyclinD-Cdk4/6 is activated in phosphorylates retinoblastoma protein (Rb) which releases E2F * E2F flat acts as a musical arrangement activator. Cyclin E-Cdk2 then phosphorylated even more Rb/E2F via positive feedback twine 17) Overview of mammalian have got points, p53 (Figs. 20-34 and 20-35)