Term
| Ames microsome mutagenicity assay |
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Definition
Using a bacterial strain Salmonella enterica sv Typhimurium that has a genetic defect in the histidine operon causing it to not grow without the addition of the amino acid, histidine.
A reagent that is mutagenic is one that causes a change in the DNA sequence or genetic defect. The defect caused by a mutagen in the Ames test causes the bacteria to be able to synthesize its own histidine again by inducing a genetic change which allows the operon enzymes to be properly translated and functional or reverted back to normal function. |
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Term
| limit of resolution in microscopy and the limits of resolution for visible light compared to electron microscopy. |
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Definition
| The limit of resolution for light microscopy is 200-350nm. See stuff this size. For electron microscope .1-.2nm resolution of protein layer one molecule thick. Discovered membrane. |
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Term
| JD Robertson’s use of electron microscopy to identify the structure and thickness of cell membranes |
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Definition
| He identified the structure of cell membranes using light microscopy. He used Schwann cells, they wrap their cell membranes around neurons. Schwann cells have myelin which is a lipid. In his bimolecular leaflet picture it showed that the dark (outer) region of cell membrane are hydrophilic and made of CHONP. The light region is hydrophobic and made of just hydrocarbons. He thought that both sides of the membrane was layered by proteins, today we know that proteins stick into membrane and in some cases span through it. |
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Term
| hydrogen bonds between water molecules (intermolecular) push the phospholipids into bilayer structures |
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Definition
phospholipids will be pushed into closed spheres to get the hydrophobic tails away from the polar water to form liposomes. It is energetically favorable to have the PLBL orient this way, it allows a higher level of entropy.
Cholesterol helps stiffen! |
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Term
| difference between saturated and unsaturated fats acids. |
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Definition
| Saturated have no double bonded carbons. Unsaturated have at least one double bond. |
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Term
| why triton x-100 and SDS are able to solubilize cell and organelle membranes |
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Definition
| They displace the lipids and unfold the proteins. The nonpolar part of the detergent attacks the nonpolar fatty acid tails and the nonpolar part of the transmembrane proteins and surround them so the nonpolar region of one can’t interact with the nonpolar region of the other. |
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Term
| means that enzymes may enable specific chemical reactions between two substrates |
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Definition
They lower the activation energy. They're very specific. Enzyme can bind to both substrate molecules and orient them precisely to encourage a reaction to occur between them. The enzyme can bind to substrate and rearrange the substrate’s electrons to create partial + and – charges that favor reactions. The enzyme can strain the bound substrate molecule and force it toward a transition state to favor a reaction.
The α helices and β sheets are examples of protein secondary structure. A protein such as hemoglobin, which is composed of more than one protein subunit, has quaternary structure. A protein’s amino acid sequence is known as its primary structure. A protein domain is the modular unit from which many larger single-chain proteins are constructed. The three-dimensional conformation of a protein is its tertiary structure. Variable domain:binds non self. Constant domain: breaks the bond to non self. Ligand binding proteins don’t make new stuff, enzymes make new stuff. |
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Term
| Christian Anfinsen’s experiment and findings about folding of proteins |
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Definition
Anfinsen showed this information is inherent in the linear sequence/primary structure of amino acid residues in the peptide chain
The conformation of the enzyme represents the thermodynamically most stable state in the intracellular environment. In his experiment he denatured a protein then slowly renatured. It went back to correct shape on its own. |
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Term
| cell membrane active and passive transport mechanisms |
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Definition
| Simple diffusion, facilitated diffusion and osmosis don’t require energy and molecules move down their concentration gradients. Simple and osmosis go straight through the membrane. Sometimes osmosis through aquaporins. Facilitated use membrane proteins. Active transport requires energy, a membrane protein, and the stuff is moving against concentration gradient. Glucose- Na+ symport protein – coupled transport uses high concentration of one molecule Na+ to move another molecule glucose against its concentration gradient |
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Term
| which molecules do not diffuse across and must be transported across |
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Definition
| Large, polar, charged stuff does NOT diffuse through membrane. Small hydrophobic or small uncharged polar molecules can diffuse through |
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Term
| action potential, how it works to transmit information from one neuron to next. |
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Definition
| Neurons(nerve cells): dendrites bring in info, cell body processes it, msg relayed down axon(can be 2mm to more than 1 m in length and can be myelinated or not), message then down terminal branches of axon into nerve terminal.Nerve signaling through action potentials. They can travel great distances down axon withoutweakening. Signal has to be continuously reamplified along the way. Voltage gated sodium channels go through a cycle when propagating a nerve signal.The resting potential when no stimulus is added is -80mv. When an action potential passes sodium channels open in response to depolarlization. Sodium ions rush into the axon further depolarizing its membrane.Depolarization continues till the equilibrium potential of +40mV. Then sodium channels switch to a refractory(inactivated) state which won’t let any more sodium into the axon and the Na channel cannot open back up (this prevents the depolarization from spreading backwards along the axon). Now the membrane potential can recover quickly after an action potential has passed. Next the sodium channel goes back to the closed state when it is back to resting potential (-80mV) so it can be ready for the next action potential. Propagation is only one direction. Voltage-gated K+ channels also function in action potential |
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Term
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Definition
| Uniports only carry one type of solute. Coupled transport can be symport or antiport. Both have co-transported ion which uses the energy from flowing down its concentration gradient to help bring the molecule in (or out) against its concentration gradient. |
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Term
| Glucose- Na+ symport protein |
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Definition
| coupled transport uses high concentration of 2 molecule Na+ to move 2 molecule glucose against its concentration gradient. Glucose is taken up from the gut by glucose/na+ symporters on the microvilli of the intestinal epithelium, then released into the extracellular fluid on the other side of the cell by passive transport for use by other tissues. |
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Term
| Erwin Chargaff and his findings and two rules |
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Definition
| Erwin chargaff: rule 1 %A=%T and %C=%G, rule 2 percentage of AT and CG pairs varies between different species |
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Term
| Hershey and chase blender experiment |
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Definition
| Used virus that infects E.Coli. Labeled DNA with 32p and protein with 35s. Viruses allowed to infect E.coli then viral heads sheared off the bacteria with blender. Bacteria put in centrifuge and the infected bacteria had 32p not 35s. Proved DNA genetic material. Amino acid: proteins have s atoms but no p atoms. DNA has p, no s. |
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Term
| how nucleus is disassembled and reassembled during mitosis |
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Definition
| nuclear lamina is right under the nuclear membrane. The nuclear envelope breaks down and reforms during mitosis. The phosphorylation of nuclear pore proteins and lamins helps trigger the disassembly of the nuclear envelope at prometaphase. Dephosphorylation of pore proteins and lamins at telophase helps reverse the process |
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Term
| centrosomes, □-TURCs (gamma tubulin ring complexes), cytoskeleton involved and polarity of growth. |
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Definition
| Tubulin polymerizes from nucleation sites on a centrosome. γ Tubulin ring complexes (γ-TURC) nucleate microtubule growth. The – end of the MT is embedded in the centrosome having grown from the nucleating ring. The + end is free in the cytoplasm. The MTs grow and shrink independent of each other. GTP hydrolysis controls the growth of MTs. MTs grow when the heterodimers are bound to GTP and the addition of subunits is faster than GTP hydrolysis. However, when MT growth is slow, the subunits in the GTP cap will hydrolyze their GTP to GDP before fresh subunits loaded with GTP can bind. The GTP cap is thereby lost, the GDP carrying subunits are less tightly bound in the polymer and are readily released from the free end, so that the microtubule begins to shrink continuously. It will continue to grow and shrink unless a capping protein is added. |
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Term
| dynamic instability and why it is thought to occur and increase greatly during prophase |
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Definition
| Increases because microtubules are pulling the chromosomes to the poles and moving organelles around also in preparation for cell division |
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Term
| motor proteins associated with specific cytoskeletal elements and direction of movement and energy source |
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Definition
| use ATP. Kinesin and dynein work on MTs and Kinesin walks – to + and dynein + to -. Myosin is on actin filaments (MF) and walk – to +. |
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Term
| function of kinase and phosphatase enzymes |
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Definition
| Proteins may be activated by phosphorylation or dephos. Requires enz to add or remove P groups. Serine, Threonine, and tyrosine can be phosphorylated on their OH group |
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Term
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Definition
| Acid hydrolases are enzymes. Made in ER and shipped in vesicle to lysosome. The function at acidic pH in lysosome (approx 5.0). pH of cell is 7.2. The pH of the lysosome is obtained by H+ pumps that use active transport to pump H ions into the lysosome. Autophagy is a cell eating its own parts. The organelle being autophagocized is sent to the lysosome for degradation. |
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Term
| How are misfolded proteins destroyed and recycled |
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Definition
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Term
| Explain the purpose of a cell signaling and signal transduction in multicellular organisms differ this process from transport across cellular plasma and cellular membranes. Include a statement about how cells may be specifically targeted to respond to a specific signal. |
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Definition
Cell signaling is the means of cell communication
Signal transduction is the process whereby one type of signal is converted to another
A target cell converts an extracellular signal into an intracellular signal. |
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Term
| reasons why cells might need to receive a signal from their environment |
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Definition
When a yeast cell is ready to mate, it secretes a small protein called a mating factor & yeast cells of the opposite sex detect this chemical signal and go to the calling cell
Respond to danger – immune response to fight infections
Muscle contraction – contract skeletal muscle, digest food using smooth muscle
Transmit information between cells/tissues in multicellular organisms |
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Term
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Definition
| Endocrine: cells that produce hormones as signals (example: the pancreas is an endocrine gland that produces the hormone insulin, which regulates glucose uptake in cells all over the body) |
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Term
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Definition
| Paracrine: signal molecules diffuse locally through extracellular fluid, remaining in the neighborhood of the cell that secretes them (example: many signal molecules that regulate inflammation at the site of infection or that control cell proliferation in a healing wound.) |
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Term
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Definition
| Neuronal: nerve cells can deliver messages over long distances quickly and specifically to individual target cells |
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Term
| Signal mediated cell-cell communication |
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Definition
| Signal mediated cell-cell communication: contact dependent, short range. Cell makes direct physical contact through signal molecules lodged in the plasma membrane of the signaling cell and receptor proteins embedded in the plasma membrane of the target cell. ( example: during embryonic development such cell communication allows adjacent cells that are initially similar to become specialized to form different types of cells) |
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Term
| Why do target cells have fast and slow responses to received cell signals? |
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Definition
| Rapid responses are possible because the signal affects the activity of proteins and other molecules that are already present inside the target cell, awaiting their orders (example: acetylcholine stimulating muscle contraction); where as slow cell response could be due to changes in the gene expressing and the production of new proteins ( example: cell growth and division) |
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Term
| Steroid hormones such as estrogen are able to act on intracellular receptors in the cytoplasm or nucleus rather than by interacting with cell-surface receptors. Why can this form of signaling occur rather than through a cell-surface receptor? |
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Definition
| They are hydrophobic molecules thAt pass through the plasma membrane to the target cell and bind to receptor proteins located in either the cytosol or the nucleus (intracellular receptors). When the hormone binds to the receptor it causes a conformational change and activates the protein allowing it to promote ( or inhibit) the transcription of specific target genes. |
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Term
| Explain the process of G-protein coupled receptors cell signaling using adrenaline stimulation of skeletal muscle as the ligand. What is an outcome of this signaling to the skeletal muscle cell? |
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Definition
| When we are frightened or excited, the adrenal gland releases the hormone adrenaline, which circulates in the bloodstream and binds to a class of GPCRs called adrenergic receptors that are present on many types of cells. In skeletal muscle, adrenaline triggers the rise in the intracellular concentration of cyclic AMP, which causes the breakdown of glycogen. It does so by activating PKA, which leads to both the activation of an enzyme that promotes glycogen breakdown and inhibition of an enzyme that drives glycogensynthesis. By stimulating glycogen breakdown and inhibiting its synthesis, the cyclic AMP maximizes the amount of glucose available as a fuel for the anticipated muscle activity. |
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Term
| How is the GPCR pathway turned off? How is its second messenger cAMP removed? |
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Definition
| GTP hydrolysis and inactivation occur within seconds after the G Protein has been activated. The alpha subunit has an baseline amount of GTPase activity, and because of that GTP turns back into GDP |
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Term
| GPCR signaling activates an enzyme phospholipase C. What does this signaling produce in the cell |
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Definition
| activation of phospholipase C is often referred to as the inositol phospholipid pathway, and it activates two small signaling molecules inositol1,4,5-triphosphate (IP3) and diacylglycerol (DAG) |
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Term
| Suppose that a cell gained a mutation in its G protein alpha subunit where it was no longer able to hydrolyze GTP. What might be an outcome to the cell if this mutation occurred? |
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Definition
| protein enters the cell and modifies the alpha subunit of a particular G protein in such a way that it can no longer hydrolyze it's bound GTP. The altered alpha subunit thus remains in active state indefinitely, continuously transmitting a signal to its target proteins. Causing an excessive outflow of ions and water |
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Term
| How does acetylcholine signaling through GPCR in blood vessel endothelial cells produce vasodilatation by smooth muscle relaxation? |
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Definition
| How does acetylcholine signaling through GPCR in blood vessel endothelial cells produce vasodilatation by smooth muscle relaxation? Acetylcholine is released by nerve terminals in the blood vessel wall. It then diffuses past the smooth muscle cells and through the basal lamina to reach acetylcholine receptors on the surface of the endothelial cells lining in the blood vessel. There it stimulates the endothelial cells and into adjacent smooth muscle cells to relax. |
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Term
| Suppose that a cell gained a mutation in its Gprotein alpha subunit and this caused a deletion in the portion that was bound to a lipid tail. What might be an outcome to the cell if this mutation occurred? |
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Definition
| activated GPCR activates G proteins by encouraging the alpha subunit to expel its GDP and pick up GTP. If a mutation came where it can no longer hydrolyze GTP, the altered alpha subunit thus remains in the active state indefinitely, continuously transmitting a signal to its target cell. Whatever protein that the activated alpha subunit was activating would also stay on. The secondary messenger would continue to be sent out |
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Term
| Epidermal growth factor signaling binds the EGF receptor, which is a member of the receptor tyrosine kinase family. How does binding of EGF ligand cause signal transduction and downstream effects |
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Definition
| epidermal growth factor originates from various cells and stimulates proliferation in epidermal cells as well as others. |
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Term
| Explain a consequence of a gain of mutation in Ras resulting in lack of GTP hydrolysis. |
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Definition
| Interaction with activated signaling proteins encourages Ras to exchange its GDP for GTP, thus switching Ras to its activated state. After a delay, Ras switches itself off again by hydrolyzing it's bound GTP to GDP. If a mutation happened and GTP hydrolysis was halted Ras would constantly be "switched on" and the phosphorylation cascade in which it promotes stimulating extracellular mitogens (cancers are caused by this mutation |
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Term
| The mutation in the above question occurred as a consequence of exposure to a mutagen. Which test would have detected its mutagenic property and how is its mutageniticy detected |
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Definition
| Receptor tyrosine kinases (RTKs) such as Ras also signal checking proteins such as Bad that encourages the cell to kill itself by indirectly activating apoptosis |
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Term
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Definition
| the cytokines (local mediators) and hormone receptors that rely on STATs have no intrinsic enzyme activity. They bind directly to receptors that can activate transcription regulators that are held in a latent, inactive state near the plasma membrane. STATs associate with JAKs ( which become activated when a cytokines hormone bind) which phosphorylated and activates STATs |
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Term
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Definition
| stimulate elaborate signaling cascades that require cooperation of a sequence of protein kinases to carry a message to the nucleus |
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Term
| Name the main difference between Notch signaling and JAK/ STAT signaling. |
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Definition
| Notch is an even more direct signaling pathway. In this pathway the receptor acts as a transcription regulator |
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Term
| Explain the metaphase -anaphase transition in mitosis which causes movement of separated sister chromatids to each centrosomal pole. Include the proteins involved in release of joined sister chromatids and process thought to be involved in shortening of kinetochore microtubules towards the poles (anaphase a model) and lengthening of polar microtubules (anaphase b model). |
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Definition
kinetochore microtubules grab onto DNA and move it into the cell. and promote disassembly at the + and - end
Polar microtubules promote cytokinesis by lengthening everything so the cell can cut itself in half
The release of the cohesion rings that hold the sister chromatids together begins anaphase. The cohesion linkage is broken by separase which binds to securin to form a complex and remain inactive; APC ( anaphase promoting complex) breaks the securin- separase complex up and securin is destroyed, thus allowing separase to break the cohesion linkages.
The dynamic instability of MTs increases 10 fold during mitosis because M-Cdks phosphorylate MAPs (ex. XMAP 215) which destabilizes the GTP cap |
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Term
| There are several major differences in cytokinesis in eukaryotic plant cells compared to eukaryotic animal cells. Explain these and include the cytoskeleton rearrangement for each cell type (plant v animal) used for cytokinesis. |
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Definition
Cytokinesis is the process by which the cytoplasm is cleaved in two.
Animal cell cytokinesis: the two daughter cells are separated by contractile rings and the remaining interpolar microtubules form a central spindle
Plant cell cytokinesis: plant cells are surrounded by a cell wall (they do not change shape), the two daughter cells are separated by the construction of a new wall. The phragmoplast guides the structures and is formed by the remains of the interpolar microtubule. These MTs guide the Golgi derived vesicles containing new cell wall material towards the middle of the cell. These vesicles fuse to form a growing cell wall that is built from the inside out. |
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Term
| The mitotic metaphase- anaphase transition is a cell cycle checkpoint. If a cell has mutant mitotic arrest defective (Mad) protein that is not functional then explain the defect that may result in the daughter cells and why the defect likely occur |
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Definition
| MAD produce a defective protein and failure of the checkpoint. The cell finishes mitosis but produces daughter cells with too many or too few chromosomes (aneuploidy) |
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Term
| A cell contains the enzyme separase which has gained a genetic defect and no longer is properly folded and cannot function. If the cell was signaled to enter G1 in the cell cycle then what would you predict would occur |
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Definition
| Separase cuts the cohesion rings in metaphase. If the separase is defective, then the cohesion rings cannot be cut in metaphase. The chromosomes will not be able to separate, and the metaphase-anaphase checkpoint sends the cell into apoptosis. |
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Term
| Frogs undergo apoptosis during metamorphosis from tadpole to mature adult. What steps most likely occur to activate this lethal system? What evidence would I see, using various methods such as microscopy, which demonstrate the tadpole cells had become apoptotic? Include the means that apoptotic cells are removed in an organism |
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Definition
The caspase family of protease and gives a response to promote apoptosis. A cell that undergoes apoptosis dies neatly without disturbing neighboring cells, the entire cell collapses changing the cell surface dramatically and signaling a macrophage
Apoptosis – programmed cell death is needed for tissue remodeling during embryonic development. Can happen directly by a death signal ( Fas/FasL) or indirectly by withdrawal of survival factors.
You would see cytoskeleton collapse, chromatin compaction, and cell volume shrinkage, breakup of nuclear envelope, nuclear fragmentation, membrane blebbing, and cell fragmentation. The apoptotic cell is disposed of by phagocytosis by another cell. The apoptotic cell Induces phosphatidylserine to be flipped by flippase from inner leaflet (cytosolic side) to outer leaflet plasma membrane which lets macrophage know that it’s supposed to eat it.
Caspase: family of proteases. Cysteine in active site. Aspartate in target protein to be cleaved. Two procaspases are cleaved and assemble into 1 activated caspase molecule.Cyt c is released from mitchondria inner membrane by activity of activated Bax or Bak
Caspase 9 causes a caspase cascade which will cause cell to die by apoptosis. Bcl-2 promotes survival of cell by blocking Bax/Bak from releasing Cyt c from mitochondria which interferes with formation of apoptosome and activation of other caspases. Progression through cell cycle depends on concentration of cyclins which regulate activation of cyclin-dependent kinases (Cdks) |
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