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Part 4 Cellular Biology Summary

by: Jewelle Williams

Part 4 Cellular Biology Summary Bio 300

Marketplace > Virginia Commonwealth University > Biology > Bio 300 > Part 4 Cellular Biology Summary
Jewelle Williams
Virginia Commonwealth University

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Book: Essential Cell Biology, 4th Edition Author: Bruce Alberts Chapters 16, 18, and 20 Summary of these chapters from notes, class and powerpoints. I used this to study for the fourth test.
Cellular and Molecular Biology
Dr Teshelle A. Ponteen Green
Biology, cellular biology, Molecular, Chapter, cell communication, Cell Signaling, ion channels, Hormones, pathways, Signal transduction
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This 12 page Bundle was uploaded by Jewelle Williams on Sunday July 24, 2016. The Bundle belongs to Bio 300 at Virginia Commonwealth University taught by Dr Teshelle A. Ponteen Green in Summer 2016. Since its upload, it has received 30 views. For similar materials see Cellular and Molecular Biology in Biology at Virginia Commonwealth University.

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Date Created: 07/24/16
Test 4 Chapters: 16, 18, 20 Chapter 16 Cell Signaling: Stages of Cell signaling:  Stage 1: Reception o Signaling mechanisms: (which start Reception)  In the absence of any type of cell signaling most animal cells are hardwired to die  Endocrine “Long distance signaling”- uses hormones as the lgand that starts a cell signal  Homones are released and transported via the blood stream  They are HIGHLY SPECIFIC to their receptors and their receptors have different functions/methods of processing in different cells  Ex: ACH o In your heart: it acts a pacemaker decreasing your heart rate o In Salivary glands it stimulates the relase of more saliva o In skeletal muscle it promotes contraction  Ex: Asprin/Naproxen/Ibuprofen: All do similar things however ______ acts as a _______ aswell illuminating its fever reducing properties to negligible at best  Contact Dependent Very Short Distnace Signaling: Cell-to-cell relay of signal ligands that require cells to touch for the signal to be relayed  Paracrine and autocrine (self signaling)- Medium Distance Signaling. The relay of signal ligands into the surrounding extracellular fluid allowing other cells (paracrine) and sometimes themselves (autocrine) to receive the signals.  These signals often produce proliferation, healing of cuts, and survival of cancer cells who often use autocrine signaling to proliferate  Synaptic: Medium distance Signaling (because axons are so long)- relay of an AP down an axon then a neurotransmitter across the synapse that either triggers another AP on that neuron or inhbits the production of other AP  Extracellular Signal molecules: Bind at the cell surface because they are either to large or hydrophilic to go through  Nuclear Signal Molecules- Molecules that are small enough and/or hydrophobic enough to diffuse through the membrane and work with either enxymes in the cytosol or receptors on/in the nuclear envelop  Ex: Steroid Hormones (cortisol, testosterone) and Thyroid Hormones  Nitric Oxide Pathway: o AcH binds to the receptor protien in endothelial (blood vessel) cells producing Activated NO synthase o Activated NOS converts Arginine to NO gas o The NO gas diffused across the membrane of the cell into the smooth muscle cells and binds to guanylyl cyclase o GTP is converted to cyclic GMP causing relaxtion of the Smooth muscle cell  Signaing Response:  Rapid: Wokds on already produced protiens to alter their function via inhibition or promotion seconds to minutes o Rapid respinsed are exspriimented with using ____________________  Slow: Works via gene expression can act as a transcription factor to prevent or promote the production of a particular gene that codes for a protien that produces the response that we do/don’t want minuetes to hours to days/weeks o Slow signal responses are exspriimented with using ______________________________________  Cell Signal Cascades:  The ligand binds to the receptor  Which promotes the production of other intracellular signaling molecules  Those molecules activate effector protiens (Metabolic enzymes/Cytoskeletal protiens/transcription regulators)  The effector protiens give you the response of (altered metabolism/alted cell shape or movement/altered gene expression)  A ligand binds to the receptor protien in either the plasma membrane (___) the cytosol or the nuclear envelope (___)  The bidning of the receptor molecule is highly specific and depending on what receptor the receptor protien binds to you will get different responses/methods of transduction (Ach in heart vs a nerve)  Stage 2: Transduction o The interemediary steps between extracellular signals and intracellular response that produces second messengers that : relay, amplify, propagate, integrate, and distribute signals through the cell o 3 types of Cell Surface receptors: (after being received transduction occurs)  Ion-channel receptors- Most straight forwars:  The signal molecule minds to the _______ sites on the channel allowing a particular ion/molecule/whatever to enter the cell via the channel and produce a response  G-protien regulation: o Effector: Adenyl Cyclase- produces small intracellular signaling molecule (second messenter) Cyclic AMP (cAMP)  cAMP signaling breaks down glycogen (sugar fat):  Avter the 7 transmembrane protien activates the G-protien complex Activated Adenyl cyslase is activated by the Gs protien subunit  Adenyl Cyclase (effector) procudes cAMP molecules wiich activates PTK  PTK phosphorylates phophorylase kinase or goes in the nucleus and phophorylaates a transcription regulator  Phophorylase Kinase phosphorylizes glycogen phophyrylase/The transcription regulator binds to DNA  Glycogen Phophorylase breaks down glucose/Transcription of the target gene o Gq alpha activates Effector Phopholipase C which produces second messengers IP3 and DAG.  IP3: Triggers release on intracellular Ca2+  The G-protien complex is activated via the 7 transmembrane protien bidning to a signal molecule and changing conformation  The Activated Gq activates phospholipase C which activates IPS (which is attached to DAG).  IP3 binds to a Ca 2+ ionchanell in the ER or SR and Ca+ is released to and Binds to activated PKC (bound to DAG on the plasma membrane) generating an AP or contraction???  DAG Activates Protien Kinase C (PKC), it remains in the plasma membrane o Those molecules produce  G-protien-coupled Receptors (GPCRs): Trigger production of intracellular messengers.  A single 7 transmembrane protien with 2 binding sites (one for the ligand and one for the G protiens inside the cell) work with a set 3 G protien subunits work together with to relay a signal. o G-protien Subunits:  Alpha: Attacheted to the plasma membrane via a lipid. Binds to GTP/GDP and acts as the switch. ~20 types  Gs is stimulatory helps with hormone signaling for glucagon and adrenaline.  Gq activates phospholipase C  Gi is inhibitory (adenylyl cyclase)  G alpha Decreases the heart rate by causing the K+ channels to open making it more difficult to generate AP and slowing down the heart  Beta:  Gamma: Lipid linked to the the plasma membrane  The process: o When inactive G alpha is bound to GDP. o When a molecule binds to the transmembrane protien and causes a conformation change ( in the transmembrane protien) that causes the g alpha’s affinity to GDP to decrease and GDP is release o GTP then binds to the site hwere GDP was activating the complex and separating G alpha rom G beta/gamma o After the targeted response is illicited the G alpha inactivates itself by hydrolyzing the GTP to GDP via its GTPase activity  Molecular Switches are governed one of two ways o Phophorylation where protien kinase covalently binds a phophate, and protien phophotase reomoes that phophate  Signaling by GTP-binding protiens  Active Monomeric GTPase o GTP-binding protiens with are signaled via GTP and inactivated by the hydrolysis of GTP to GDP  Example Disease: Cholera: o A gastrointestininal disase that can cause death o Cholera Toxin prevents Galpha from hydrolysig GTP in the gut cells. o This propagates to production of anylate cycleas  cAMP forcing Cl- out of the cell causing dehydration and loss of nutrients (which can lead to death) o Whooping cough (pertussis)- alters G alpha subunit Gi and inhibits adenyl cyclase  Signal Amplification: o Via a cascade effedt??  Enzyme coupled Receptor (RTKs): Trigger the activation of a series of protiens  Receptor Tyosine Kinase phosphorylate protiens at tyrosine resudues o RTK (which is phosphorylated) binds to the singnal molecule o An adaptor protien binds to a phophate and activates Ras-GEF o Ras-GEF decreases Ras proteins affinity for GDP allowing it to be activated by GTP o Ras Protien activates MAP 3K o MAP3L activates MAP2K o MAP2K activates MAPK o MAPK activates either protiens (which changes protien activity) or Transcription regulators (which alters gene expression)/Activates Akt o Akt phosphorylates Bad protien promoting inhibition of apoptosis  Highly influenced by the cell cycle migration/metabolism/proliferation   All are governed via Negative or Positive Feedback systems  Positive: Feeds back into its own process and amplifys the result  Negative feeds back into its own process to inhibit the result  Response Chapter 18 Cell Cycle:  There are 2 types of Nuclear Division o Meiosis- Division of germ cells for the production of new (multicellular) organisms o Mitosis- Division of somatic cells (for growth and development of organisms)  Focus of this chapter  Mitosis: o Divided into 2 phases with subphases o Each phase varies in length o The total time length varies from organism to organism/type of cell o Identical daughter cells are produced o Go-ahead signals:  External: Growth factors (cytokines and hormoes)  Internal: Promoting factors  Cyclin- regulatory protiens  Regulated by ubiquitination for drestruction via Anaphase promoting complex  Cdks-cyclin dependent kinases  Activation of Cdk drives the cell cycle  Cdk-cyclin complex- promoting factor triggers entry entry into S or M phase  Phophorylation inactivatesx the complex until the activating phophotase is activated and inactivates phophotase  P27 for inactivation of the complex o Check Points:  G1/S-phase: IS the environment favorable?  G1 Arrest: DNA dammage activates p53 which activates the transcription of p-21 protien, a protien that inactivates G1/S-Cdk and S-Cdk  S/G2-phase: Is all DNA replicated? Is all DNA dammage repaired?  G2 Arrest: M-Cdk remains inactivated via phosphorylation because Cdc25 is inhibited by DNA dammage  During M-phase: Are all chromosomes properly attached to the spindle? o Interphase- the phase of growth, replication, duplication etc all in preparation for M-phase  90% of the cell cycle  Phases:  G1-phase- 7-9Hours  This phase begins the cell cycle  Mitogens (external signals) activate G-CDK and G1/S-CDK which phosphorylate active Rb  Once phosphorylated Rb becomes inactive and releases the transcription regulator on DNA allowing S-phase to begin  Allows the transcription of genes  S-phase- 6-8 hours  DNA replication begins due to the release of the transcription regulator (Rb protien)  Origins of replication (ORC’s), which are present al through the cell cycle, recruit Cdc6 to the DNA strand. Cdc6 loads helicase on the DNA strand and “loads” the DNA strand for replication  S-Cdk pulls the trigger and when it activates S- phase where the replication occurs  Along with DNA duplication centrosomes are duplicated aswell  G2-phase- 4-5 hours o M-phase-Dephophrylation of M-Cdk by phosphorylated Cdc25 drives the cell to M-phase via positive feedback.  Prophase- Chromosomes condense (condensing) and the Sister phromatids are held together with cohesion rings  Centrosomes move apart and begin to form their spindle:, interpolare microtubules attach to each other, Aster microtubules start to grow  Prometaphase  The nuclear envelope is proken down via phosphorylation of the nuclear lamins  20-40 Kinetochore microtubules attach to kinetochores on the sister chromatids  Metaphase  Begins when the chromosomes are aligned at the equator of the cell  Once aligned Kinesisn motor protiens start to pull the chromosomes in opposite direction (bi-orientation)  Seperase is Activated by APC, which tags securin for ubiquitination.  Anaphase  Begins when Seperase is active  Seperase cuts the cohesion rings allowing the kinesin to pull the sister chromatids (now chromosomes) apart to opposite sides of the cell (-)  Dynamic instability also plays a part in the shrinking of the microtubules as the chromosome is pulled to the centromere  Cleavage furrow forms midway between interpolar microtubules  Telophase  The depolymerization of the lamins and nuclear envelope allows a nucleus to form around the chromosxomes on each side of the cell  Chromosomes decondense  Cytokinesis  Actin filaments attached to the inner plasma membrane and shrink intil there are 2 identicle daughter cells  The actin/myosin complexs then disentigrate Cell Size and Number:  There is a dynamic balance between cell death and proliferation  Cell Death can happen one of 2 main ways: o Apoptosis: Controlled Cell death  There is no effect to surrounding cells  The remaining cellular material can be recycled  Incactive procaspases initiate caspase  The protiens responsible for proliferation and apaptosis come from the same family  Bad, Bax death relase cytochrome C from mitochondria and activate caspase  Bcl-2 life/proliferation blocks cytochrome C release  The process:  Cytochrome C attaches to an adaptor protien and they assemble  The complex recruits procapspase-9 molecuels and create an “apoptosome” which causes an irreversible caspase cascade leading to apaptosis o Proliferation/Growth:  Bcl-2 promotes growth by phophorylating Bad and relasing active Bcl-2 (inactivated by being in a complex with Bad) and blocking apoptisis  Growth factors increase protien synthesis and decrease protien degredation o Necrosis: Acute Injur  This often happens as a result of “overdose” in some chemical  This form of cell death causes dammage or death to surrounding cells Chapter 20 Cell Communities; Tissues, Stem Cells, and Cancer  There are 4 types of Tissue in Animals: o Epithelial Cells (skin) o Connective Tissue o Muscle Tissue o Nervous Tissue  Connective Tissue: Fibroblasts: o Most abundant and diverse tissue o Provides Tensile Stregnth o Types of CT:  Dense CT  Loose CT  Areolar T  Bone  Blood o Main functions:  Support  Defence- blood and lymphatic  Transport  Storage  Repair o Fibroblasts: Secrete Collagen into extracellular matrix  Collagen  is a strong molecule secreted by fibroblasts into the extracellular matix  is secreted as “procollagen” and is converted to collagen by procollagen proteinases that cleave it into collagen  structure: Single polypeptide chainTriple-stranded moleculeFibrilFibers  Provides tensile strength  20 types, 25% of the total protien in mammals  Ehlers-Deanlos Syndrom- lacks enzyme that converts procollagen to collagen o It’s a loosely packed cells in fibers and gels (extracellular matrix) o Function:  Support  Defense  Transport  Storage  Repair o Binding/Restructuirng Collagen in matrix:  Requires Integrins, fibronectin, adapor protiens and active filaments  Starting in the cell to the outside of the cell:  Actin filaments are attached to adaptor protiens  Adaptor protiens are attached to integrins (transmembrane protiens)  Integrins attach to fibronectin which has 2 types of attachment sites o Collagen binding which bind to collagen o Cell attachment site Attach to the integrins  Fibronectin attach to the collagen fibril o Intefrin Signaling:  There are 24 types of integrins in humans  Structure: 2 subunits work together an alpha and beta subunit  When inactive they are “coiled” together close to the plasma membrane  When active they are extended into the extracellular matrix o Proteoglycans:  Negatively charged GAG’s that link together to form proteoglicans  The GAGs are linked to a coreprotien and form large aggregates  Very hydrophilic and tend to have exstended conformations that occupy large volumes  They are resistant to compression and when combined with collegen can form very tough resilient structures (cartiledge)  Junctions and the Epithelium: o Function: Secure cells to each other via various means o Tight Junctions o Desmosomes o Hemidesmosomes o Gap Junctions o Epithelium:  lines surfaces and organs in the airway, urinary and digestive track and the skin  Secretes hormones tears and milk and transports nutrients and waste  Has receptors and facilitates cell movement  Little of no intracellular matrik  Uses Cell-Cell Junctions  Tight Junctions: structures that seal neighboring cells together so that water soluble molecules cannot easily pass between o Found in gut lumen and intestines  Adherins Jundtions join actin bundles from one cell to a neighboring cell o It is an adhesion belt that can be used to form the lens or neural tube in embryonic development o Uses cadherin to bind o Actin filaments  Desmosomes join cells together using cadeherins wheich are attahched to intermediate filaments o Strength, distribution of shocks o Many cadeherens join together providing a gough secure bond o Found in tough tissues like the skin and intestines  Gap jundtions allow transport of molecules/charges between cells o Allows coupling of electrochemical and metabolic process o Can transport ions water small molecules and action potentials (in heart) o Signaling regulates the permeability. Dopamine reduces the gap junction communication o Signals also tell the regina to switch between rods and cone in our eyes  Hemidesmosomes anchor cells to the basil lamina via intermediate filaments (keratin) and integrins o Blisters are a esult of the disruption of theses  Basil membrane:  A separation point between epithelium and CT  Basila lamina is formed from type 4 collagen (IV) and laminin protien (the fibronectin of the epithelium)  Tissue maintenance and renewal: o Tissues are organized into layers and have different components based on the function they provide and their location  Ex: Skin: EpidermisLoose CT Dense CT Hypodermis  Epidermis is a made up of several layers of squamis cells (Stratified) with keratin and melanin  Loose CT helps secure the basal cell of the epidermis, contains a moderate amount of proteoglycans (GAGS) that are sticky  Dense DT contains nerves and blood vessels, contains a large amount of collagen fibroblasts and elastic fibers making this more tough and dense  Hypodermis is made up of o There are 3 Main features that allow the stability/renewal of tissues  Cell Communicaiton via cell signaling  Slective Cell-cell Adhesion-  Cell Memory- specific gene expression (specifically in differenciated cells)  Stem Cells:  Self-renewal  Precursur cells become differenciated  Small number of dividing cell that divided endlessly o Ex: Intestines the cells are constantly being renewed there are layers of cells stem cells, precursor cells, Mature cells (terminally differenciated) o Ex: Skin: the dividing basal cells (proliferating and precursor) move upwards to the skins surface and are shed o WNT signaling pathway: signals the proliferation stem cells in the small intestines  Active-APC degrades beta catenin preventing the transcription of genes and turning off the Wnt responsive genes  Hematopoisis: o The production of blood cells from stem cells in the bone marrow o Cancer  Tumors:  Benign Tumors are noncancerous clusters of cells o Hyperplasia and dysplasia  Malignant Tumors are cancerous masses that can metastasize and from secondary tumors  Cancer Risks:  1 in 2 men get cancer  1 in 3 women get cancer  You are most likely to die from pancreatic cancer  Progression:  Normal Cells (reproducing properly)  Hyperplasia: increase in the number of cells  Dysplasia: abnormal growth of cells with loss of cellular orientation shape and size compared to normal tissue  Cancer: Mutated cells that proliferate indefinitely  Risk factors :  Genetic instability: Free radicals, smoking, gas fum o Defects in DNA replication, repair, cell-cycle checkpoint  Mistakes in mitosis  Abnormal chromosome numbers  Age: more tim to accumulate mutations o You get one mistake for every 10^9 or 10^10 nucleotides replicated  It is a step wise process. o One mutation produces another mutated cell (if it is not triggered to apoptosize) etc  Oncogenespromotes tumors  Come from Anti-oncogenes  Mutations in Rb (inactive mutation) and p53 (active mutation) drive proto-oncogenes causing cancer  Anti-Oncogene tumor suppressors  They have reduced dependence on signals for growth survival and division  They continuously replicate and have little or no actions to apoptisize  They have GTP contantly attached to the Ras triggering replication  They block apoptosis by producing Bcl2 protien unlimitedly  GTP is bound to ras protien (active) continuously causing proliferation  Angiogenesis: the ability to grow their own blood vessels  Abnormal Cadherin protiens that promote growth in new areas  Stage force:  Cancer in most of liver, _____________, ______________  Treatments:  Radiation kills rapidly dividing cells  Sugery  Chemotherapy o Stops DNA replication, mitosis, cytokinesis and angiogenesis  Vaccinations  Kinase inhibitors for Adult leukemia and stomach cancer- prevents the attachment of ATP to kinase in cancer cells  Gene therapy


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