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Cell Biology

by: Annette Leannon

Cell Biology BIO 4301

Annette Leannon
Florida Tech
GPA 3.97

Julia Grimwade

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Julia Grimwade
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This 51 page Class Notes was uploaded by Annette Leannon on Monday October 12, 2015. The Class Notes belongs to BIO 4301 at Florida Institute of Technology taught by Julia Grimwade in Fall. Since its upload, it has received 10 views. For similar materials see /class/221686/bio-4301-florida-institute-of-technology in Biological Sciences at Florida Institute of Technology.

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Date Created: 10/12/15
Cell signaling Communication between cells Direct cell contact Secreted molecules that either go into blood endocrine or diffuse between cells paracrine A cell can also send a signal to itself autocrine There is also intracellular signaling The components of the system Signaling molecule Receptor of the signal Molecules that transmit the signal to ultimately generate an effect Direct CelICell Signaling i Signaling by Secreted Molecules A Endocrine signaling B Paracrine signaling 39 i f V r 7L4 rm l Fan 0 Frm39 Signaling molecules Lipid soluble can pass through a lipid bilayer These have intracellular receptors Water soluble can t pass through a lipid bilayer These have cell surface receptors Lipids that although hydrophobic still bind to surface receptors Lipid soluble intracellular receptor Steroid hormones Receptor in the cytosol Nuclear receptor ligands thyroid hormone Vitamin D Retinoic acid Receptor is in the nucleus usually bound to DNA Receptors as transcription factors The steroid hormone and nuclear receptor superfamily members are transcription factors The DNA sequences they bind are often called Hormone Responsive Elements HRE The activity of the factor is regulated by binding to the signal We have already seen the example of the steroid hormoneglucacorticoid receptor Receptor is held in cytosol because it is bound to a chaperone which keeps it slightly unfolded and masks its NLS Binding of hormone changes the conformation of the receptor which is released by the chaperone The conformation change reveals the NLS so the receptorhormone complex is carried to the nucleus where it binds to cisacting regulatory sequences on specific hormoneresponsive genes The conformational change also allows the receptor to dimerize and allows the activation domain to work The activation domain recruits a HAT or other coactivator which changes the structure of the chromatin Estrogen O Plasma membrane Another view Hormone enters cell binds to ligand binding domain LBD of the receptor The binding changes the Hormone conformation of the LBD and causes the LBD to be released from tethering proteins inhibitors that block the NLS and prevent transport into the nucleus The hormone bound receptor now has an exposed NLS and can now associate with importin and get into the nucleus In the nucleus the DNAbinding domain blue and the activation domain green function to regulate gene expression Binding of hormone is needed for this to happen too The receptor is always bound to the cisacting regulatory sequence of the gene In the absence of hormone the receptor acts as a gene repressor because it has a repression domain that recruits a HDAC or other corepressor which causes chromatin condensation When hormone is added the hormone binds to the ligand binding domain of the receptor This changes the conformation of the receptor so that the repression domain is no longer functional and an activation domain appears instead The activation domain recruits a HAT or other coactivator l 11mm Immune l Thyroid hormone receptor i L is i la r A I Transcription repressed O Hormone added NW Acetyl grm l gtTranscription activated THE CELL Faun Edition gure 15 2003 ASM Press and Sumner n Cell surface receptors These bind to signaling molecules that can not pass through the plasma membrane Examples would be neurotransmitters neuropeptides peptide hormones and peptide growth factors Neuropepetides include endorphins which were found because scientists were puzzled as to why we had a specific receptor for morphine Peptide hormones include insulin pituitary factors Peptide growth factors include most molecules that regulate development growth and cell cycle Binding of the signal to the receptor changes the conformation of the receptor The conformational change can Cause a membrane ion channel to open Activate an enzymatic activity either directly or indirectly Neurotransmitters Acetylcholine 0 H CH3 c o CH2 CH2 N CH33 Glycine II H3N CH2 C O Glutamate H3N CH CHZ CHZ C O 04 Dopamine HO HO CH2 CH2 NH Norepinephrine HO HO CH CHz NH OH Epinephrine HO HO CIH CHZ NH CH3 OH Serotonin HO CHZ CHz NH N I H Histamine HC C CH2 CHZ NH N H K y Aminobutyric acid GABA I H CHz CH2 CH2 C O THE CELL Faunh Edirian Figure I56 Q 2006 ASM Press and SinauerAssocwates inc Many neurotransmitter receptors are a ligandgated ion channels Binding of the ligand neurotransmitter opens the channel letting a rush of ions to pass through the channel The best studied of these is the nicotinic acetylcholine receptor shown here This receptor can be found on muscle cells In the closed state the channel is closed because hydrophobic side chains interact in the center of the channel closing it When acetylcholine binds there is a conformational change and the hydrophobic side chains move out of the way opening the channel to Na and K ions There is more Na outside the cell and so Na rush into the cell This depolarizes the plasma membrane of the muscle cell triggering an action potential which is really the successive opening of voltagegated ion channels The action potential ultimately results in the opening of voltagegated Ca channels increasing cellular calcium which causes muscle contraction Neurotransmitter S Outs39de P ore Acetylcholine binding site inside Gate THE CELL Founh Edition gure v32a o Called a nicotinic receptor because nicotine keeps it open all the time Some snake venoms and curare are inhibitors of the channel and keep it closed Motor Voltagegated neuron Ca2 cha nnel Acetylcholine J Nicotinic l Caychannel acetvlcholine receptor 3 TmbUle 39 i x Na ca L Voltagegated Na chan nel Na39 Sarcoplasmic 1 I Muscle cell r reticulum 32 release channel Surface receptors that are indirectly linked to enzymes How are signals transmitted from the cell surface receptor Activation of enzymatic activity either directly on receptor or indirectly through an intermediate There are a bunch of intermediary proteins that act in signal transduction Some of these are called second messengers Often the signal transduction involves a cascade of events and amplification of the signal Receptors linked to Gproteins This is a big class of surface receptors Neurotransmitters neuropeptides peptide hormones sensory receptors all fall into this class Also lipids that do not go through the membrane called eicosanoids involved in immune system have this type of receptor Gprotein linked receptors 0 Receptor has 7 Extracellularside transmembrane Carbohydrate domains The ligand binding site is in the extracellular domain The cytosolic side is associated with a trimeric Gprotein Cytosolic side A trimeric Gprotein has three subunits The ocsubunit binds the guanine It can bind either GDP inactive or GTP active The B and y subunits are generally regulatory When the ligand binds the trimeric Gprotein associated with the receptor undergoes nucleotide exchange and the GDP is exchanged for GTP thus activating the G0 The G0 diffuses off to associate with a target protein whose activity is regulated by the G protein G0 is inactivated by hydrolysis of GTP to GDP Hydrolysis is by an intrnsic GTPase but cab be stimulated by a GAP Target of some bacterial toxins O Hormone 0 Exterior Inactive Trimeric Gs protein w c t I receptor ff G 050 q T v V Gm P G G 3 Binding induces conformational change in G bound GDP 5 P dissociates and is replaced by GTP G X dissociates from Gm Q U I Binding of hormone induces a conformational Hormone dissociates from receptor Gubinds to effector change in receptor activating it G S S w P P Activated receptor binds to Q1 subunit Hydrolysis of GTP to GDP causes Guto dissociate from effector and reassociate with Gm Human genome has 27 different GOL 5 different GB and 13 Gy The GOL are divided into classes depending on the function of the effector target TABLE 131 Major Classes of Mammalian Trimeric G Proteins and Their Effectors quot Gty Class Associated Effector 2nd Messenger Receptor Examples Gm Adenylyl cyclase CAMP increased B Adrenergic epinephrine receptor receptors for glucagon serotonin vasopressin Gm Adenylyl cyclase CAMP decreased ml Adrenergic receptor K channel GEW activates Change in membrane Muscarinic acetylcholine effector potential receptor GUM Adenylyl cyclase CAMP increased Odorant receptors in nose G qu Phospholipase C 1P3 DAG increased aZ Adrenergic receptor Goa Phospholipase C 1P3 DAG increased Acetylcholine receptor in endothelial cells Gm CGMP phosphodiesterase cGMP decreased Rhodopsin light receptor in rod cells A given Gm subclass may be associated with more than one effector protein To date only one major Gm has been identified but multiple Ga and Gm proteins have been described Effector proteins commonly are regulated by Gm but in some cases by GM or the combined action of G and Gm IP3 inositol 145 trisphosphate DAG 39I2 diacylglycer0l SOURCES See L Birnbaumer 1992 Cell 7121069 Z Farfel et al 1999 New Eng I Met 34011012 and K Pierce et al 2002 Nature Rey Mol Cell Biol 3639 The targeteffector proteins are adenylyl cyclase makes CAMP phospholipase C makes P3 and DAG or CGMP phosphodiesterase Some Goa are stimulatory GSoc some are inhibitory Gioc Some GBy can activate ion channels What cyclic nucleotides can do Cyclic nucleotides are CAMP or cGMP They are made by adenylyl or guanylyl cyclases and degraded by phosphodiesterases Goa can activate cyclases inhibit cyclases or activate phosphodiesterases Cyclic nucleotides act as second messengers and amplify the signal caused by the ligand hitting the receptor The target of the second messenger can be an ion channel vision olfactory system or an enzyme The enzyme is generally the kinase protein kinase A Olfactory neurons work using receptors linked to trimeric G proteinsthe GOfoc indirectly opens ion channels Olfactory receptors in the nose are on the surface of cilia extending from the olfactory neurons There are over 1000 different receptors that work in combination to detect different odors When an odorant binds the receptor activates a Golf which then activates adenylyl cyclase which makes CAMP The CAMP then binds to a ligand gated ion channel for Na which o r oCHz o Adm causes an influx of Na resulting 0 in an action potential that travels along the axon to the brain Phermone detection is similar but uses phermone receptors rather than olfactory receptors CAMP activation of protein kinase A Receptor binds ligand The binding causes receptor to gediate exchange of GDP for GTP on 06 Goa activates adenylyl cyclase and makes CAMP CAMP binds to PKA and activates it PKA has two regulatory subunits R and two catalytic subunits C Binding of cAMP removed the regulatory subunits releasing the active kinase catalytic PKA is a serinethreonine kinase and phosphorylates serine or threonine quot1 residues on target proteins Active I Classic example is glycogen metabolism activated by epinephrine fight or flight response What the response is depends on the particular isoform of PKA and the substrates in the cell Gene activation by CAMP The C subunit of PKA has an NLS masked by the R subunit When CAMP causes release of the Protein C subunit it can go into the kinaseA l nucleus There it can phosphorylate a transcription factor called CREB CREB is a leucine zipper factor Phosphorylated CREB binds to the cAMP responsive element CRE in the promoter of some genes CREB stands for CRE binding protein When CREB is phosphorylated it becomes a transcriptional activator capable of binding co activators The coactivator of CREB is called CRB which has HAT activity and can recruit more HAT s as well as bind to basal transcriptional machinery Cytosol Inactivation of PKA Remember phosphodiesterase will convert CAMP to AMP Things that inhibit phosphodiesterase can prolong the effect of the stimulus There are also protein phosphatases that remove the phosphate put on by PKA Signal amplification One ligand here epinephrine is shown I d t Epinephrine 10 M Amplification swntleigs39soof rian Ait y I y H I cyclase CAMP molecules ammo 5M These in turn will a a a a a P activate multiple PKA Amplification enzyme phosphorylate even more targets Trimeric G proteinsreview Directly activate ion channels3y subunit Activate cGMP phosphodiesterase vision Activate adenylyl cyclasemake cAMP Activate PKA Bind to ion channelolfactory system Activate Phospholipase C B Make inositol triphosphate and diacyl glycerol Phosph olipase C There are al least two isoforms and PLC y PLC B is stimulated by a Goa subunit of gt a trimeric G protein PLC cleaves phosphotidylinositol 45 biphosphate PIP2 PIP2 is a phospholipid found in the inner leaflet P39P2 of the plasma membrane Cleavage of PIP2 yields two products both with activity as second messengers Diacylglycerol DAG remains in the membrane lt activates protein kinase C PKC family members PKCs are serine threonine kinases lnositol 145 triphosphate ng is ON released into the cytosol where it goes quotdo3 to ligandgated Ca channels and opens them resulting in a rush of Ca into the cytosol The calcium is usually stored in the endoplasmic reticulum or outside the cell The cytosolic calcium levels are Eniopismicinc iuumo o o 0 usually very low kgwywv39w The DAGIP3 pathway Binding ofa ligand to a receptor activates a Goc protein which activates PLCB PLC makes lP3 and DAG lP3 goes to the ER and opens E t I itquotsp mlpaseC Ca channels Prim membrane One thing the Increased Ca cytosou does IS cause Protein Kinase C to HP move to the plasma membrane 3ch Phosphorvlation a ol subsxmss where it interacts with DAG rv PW Once active PKC has many 5 different targets depending on IP30 a mm the cell type In the liver it can a C8 quot3quot 9 regulated glycogen storage PKC also plays a role in the cell cycle 9 When the Ca levels in the ER TZ are depleted the ER channels Ca Endonasmicre cuum bind to and open Ca channels in the plasma membrane letting Ca in from outside the cell Calcium is also a second messenger Increased cytosolic calcium does more than help activate PKC Ca will bind to and activate a protein called calmodulin Calmodulin regulates a lot of other protein including more kinases One family of kinases that can be activated by calmodulin are called CaM kinases Targets of CaM kinases include transcription factors metabolic enzymes and ion channels A CaM kinase in nerve cells activates the enzymes needed to make neurotransmitters A CaM kinase can also phosphorylate CREB and activate itjust like PKA can and so can play a role in learning and memory too CaM kinase can also regulate adenylyl cyclases and phosphodiesterases This means that there is a lot of coordination between the CAMP pathways and the IP3DAG pathways Calmodulin oOo Ca2 Ca2 0 binding Ca2Camodulin Ca2calmoduin dependent protein kinase THE CELL Faurm Ediiian gure I Cerebellum is involved in implicit memory Hippocampus and medial temporal lobe are involved in explicit memory Implicit memory easier to study Basis for model system used to work out the molecular biology of learning and memory Eric Kandel Aplysia Two types of storage mechanism for both types shortterm memory and longterm memory Difference is due to strength and structure of synaptic connections Reductionism in the Neurobiology of Learning and Memory Why Aplysia Aplysia as a model of synaptic plasticity 5 marine mollusc hermaphroditic gastropod usually quiescent simple behavioral repertoire and relatively simple nervous system make it an appealing subject for studies of the molecular neuronal and circuit mechanisms of learning and memory apiysia exhibits a Vigourous withdrawal of the siphon and gill under the mantle when the siphon is touched or hit with a jet of seawater Elegant simplicity of Aplysiu few large neurons consistent cells across individuals cell bodies are on outside of ganglia so are easy to stimulate and record UF psychology dept httpwebneurobioarizonaedugronenber gnrsc581lpowerpoinPAZOpdfsIearnmemm 0pdf Sensitizing slimubus Sensory Facilitating m neuron inlemaumn E Three molecular targets involved ir presynamic laciliation Serotonin acts on two receptors Gs CAMP gt PKA Go DAG gtPKC PKA PKC 1 decreases K current IongerAP more Ca phosphorylates WW channel 22a mobilizing vesicles facilitating release 33a opening of Ca channels Facrllraung imameumn Available quot305mme Ntvpe Caquot 39 n Releasable transmitter Glutamate quot receptors httpwebneurobioarizonaedugronenber gnrs058 lpowerpoint20pdfsearnmemm 0pdf Gene activation reqUIres Nucleus W C Chromatin structure CHEM one one cm W histone acetylation In T 6 Em G cEBF39 activation is coupled to l a deactylation f CREEquot J G a CREB transcription factors Ub qui iquote C EEP are not the only ones tp play a role EH NMDA AMPA NMDA AMPA Notjust slugs Drosophila and mammals have a very similar setup Mann awry Nan on Follower Neu ran Dulpul ma Mater Systems Gene activation requires Nucleus W Chromatin structure CHEM CRE CHE GMT WC histone acetylation In a m activation is coupled to l G c39anpo deactylation f CREE CREB transcription factors are not the only ones to play a role Tail 5HT D B Genes that are turned on not all known W Channel Ubiquitin hydrolase quot Transcription factor CEBP 39 63 which with ofther factors D turns on genes needed for AMPA NMDA synaptic growth AMPA NMDA Rolipram is a Relationship to human disease phosphdiesterase inhibitor gm gig M gt 320 A 4 WED 00639 Cell 126 775 788 August 25 2006 a2006 Elsevier Inc CHE 9 CAAT Nucleus TAAC Tail 5HT G V GOltIO AMPA NMDA J G n 055 2an t CREE1 G AFi l 1 Q a l Ubiquitin CEBP Hydrolase Growth 2 A V39I AJ W DFW AMPA NMDA How do the gene products used in growth get to the correct synapse Synaptic capture model Synapses tagged by previous activity Tagging involves PKA localization of mRNA to synapse Protein synthesis is localized because mRNA is localized and because protein translation factors etc are activated locally There is also a change in the structure of the synaptic membranes where cell adhesion molecules CAM are internalized removed This may increase synaptic growth make new synapses Apoptosisprogrammed cell death Some cells die as part of their normal developmental pathway Other cells die when they have suffered un repairable damage to DNA The programmed death or apoptosis is different from death due to acute injury or lack of blood flow necrosis Apoptosis is neat and there is no release of cellular material which can cause inflammation DNA fragmentation Chromatin condensation 1 Fragmentation cl nucleus l Fragmentalion or me tell Apupm c Activation of apoptosis Apoptosis starts because effector proteases called caspases cleave nuclease inhibitors nuclear lamins cytoskeleton etc Caspases cut at the Cterminal end of asp residues Regulator The last effector caspase in apoptosis is caspase3 Caspase3 is activated by being cleaved by another caspase called caspase 9 in some pathways caspase3 is activated by caspase8 Caspase 9 is regulated by factors that respond to death signals Effector e egans ea Vertebrates Bel2 I A f c gt Casp9 gt Casp3 gt Death Regulation of apoptosis To be active caspase9 must interact with a protein called Apaf 1 the adapter Apaf 1 can only interact with caspase9 in the presence of cytochrome C Cytochrome C is usually in the mitochondria and not around either caspase9 or Apaf 1 Controlling the release of cth by regulators is a major way ces control apoptosis Mei Effector Regulator C elegans CEDS I USS 504 gt CED3 gt Death Vertebrates Bel2 ItN iiiii1quot gt Casp9 gt Casp3 gt Death Cytochrome C Caspase 9 initiator caspase Apaf l Pro caspase 3 Active caspase3 Effector caspase Cleavage of nuclear lamins cytoskeletal proteins DNase inhibitor The Bcl2 family The regulators of cth release are members of a family of related proteins called the Bc2 family Some family members promote apoptosis Brelease of cth an example of this would be ax Some family members promote survival retention of cth in the mitochondria an example would be Bcl2 Those that promote death cause release of cth from the mitochondria Those that prevent death cause retention of cth in the mitochondria This is a simplified scenario Bax oligomers increase permeability of mitochondrial x membranes so thatcth can be released How Channel is hypothetical Bcl2 can bind to Bax and l J P prevent it from promoting gt 3 r Pro caspase3 Active caspase3 cth release IAP inhibit caspases Smac Antiapopt tic ixlul domain protein proapoptotic promote apoptosrs M protein Bax In addition to Bax there are other family members in this slide called BH3 only proteins that promote apoptosis by binding to Bol2 and preventing it from inhibiting Bax Examples of these are Bad PUMA and Noxa Apoplutic cell Cell death signal Activation of BH3eonly pro ei proapoptotic t n What causes cells to enter apoptosis DNA damage If cells are damaged then induction of p53 will stop the cell cycle and allow time for repair If the damage is severe the cells will die rather than replicate a damaged genome P53 does this by increasing transcription of two regulators of Bcl2 PUMA and Noxa These bind to Bcl2 and prevent Bcl2 from binding Bax Bax can then let the cth out of the mitochondria DNA damage s Increased levels of p53 1 lsmum Lgt PUMA Noxa a Bind Bc2 Death signals Some cells are induced to die by exposure to a death signaling pathway This is common in the immune system and is one of the ways your immune cells kill cells infected with virus The death signal example TNF binds to a death receptor eg Fas This creates a binding site for adaptor molecules that recruit and activate caspase 8 Caspase 8 can activate Caspase 3 Caspase 8 can also activate a BH3 only protein Bid that will tie up Bcl2 and let Bax form channels in the mitochondria letting out Cth THE CELL Founh Edit Survival signals During development many cell types need to interact with survival signals in orderto survive In this case a survival factor generally a growth factor activates a receptor tyrosine kinase The phosphorylated tyrosines bind PI3 kinase which makes PIP3 V Survival factor Receptor tyrosine kinase mTORrictor Pl 3kinase Active Akt Akt binds PIP3 Active Akt phosphorylates Bad a BH3only protein that inhibits Bcl2 Bad 1 Phosphorylation of Bad creates a binding mm site on Bad for 1433 1X0 39 1433 is a protein that binds a variety of phosphorylated proteins and holds then in 3 quot the cytosol When Bad is bound to 1433 it can t inhibit Bcl2 Bc2 is free to tie up Bax so Bax channels can t form in the mitochondria and so no Cth is let out No cth no caspase 9 activation and so cells survive a Absence of trophic factor Caspase activation 3 Presence of trophic factor Inhibition of caspase activation Tro hic factor Trophic factor receptor p I Plasma membrane Death Cleavage of substrates gt I 39 quot naca39snase Outer mitochondrial membrane 39 Ions Growth factor Growth factor receptor PI 3 kinase 1433 THE CELL Founh Editian gure 1830 a zoos ASM Pr 1433 ties up Bad 1433 also ties up the transcription factor FOXO if it is phosphorylated by Akt In the absence ofAkt FOXO is free to go into the nucleus where it turns on Bim a protein like Bad Bim promotes apoptosis Apoptosis and Cancer It is important to remove altered self cells by the immune system using death signals It is also very important that cells that have severe damage to their genomes die rather than replicate Finally cells not receiving survival signals are not needed and should die rather than replicate For these reasons apoptosis is carefully regulated Loss of regulation that leads to increased cell survival generally leads to cancen Genes that promote survival suppress apoptosis are usually oncogenes Akt Pl3 kinase and Bcl2 are known oncogenes in human tumors Growth factors and growth factor receptors are also known oncogenes Overexpression of these proteins leads to survival of cells that should die and ultimately to cancer 5quot Growth factor Growth factor receptor Tumor suppressors can stimulate apoptosis We already know about p53 Another tumor suppressor is a protein called PTEN which is a phosphotase that removes the phosphate from PIP3 that was put on by Pl3 kinase Without PIP3 Akt can t be activated and the m b i survival signal is not transmitted


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