Final Exam Questions & Diagrams PDF

Final Exam  ❖ What is function of the G1 DNA-damage checkpoint? the restri...

Final Exam  ❖ What is function of the G1 DNA-damage checkpoint? the restriction checkpoint? The Cell Cycle the S DNA-damage checkpoint ? ❖ What are functions of cell cycle? the G2 DNA-damage checkpoint? ❖ What are functions of principal phases of cell cycle? the unreplicated - DNA checkpoint? the spindle-assembly checkpoint? ❖ What is / are checkpoint/s of the the chromosome-segregation checkpoint? G1 phase? G2 phase? ❖ What is the main result of the malfunction Checkpoints below listed checkpoints? S phase? M phase? The G1, S, and G2 phases of the cell cycle and the spindle assembly checkpoint at M phase; The G1 restriction checkpoint. What are aneuploid cells? What is mitotic catastrophe? What is the loss of contact inhibition? ❖ What are G0 cells? ❖ What is response to injury fulfilled by a reserve population of stem cells represented by G0 cells?  Which statement does support development of mitochondria from an aerobic prokaryote that lived What mitochondrial membrane contains the symbiotically within primitive eukaryotic cells? respiratory electron-transport chain, synthesize ATP, and regulate transport of metabolites into and out of Where are the enzymes for.-oxidation of fatty acids the matrix? located in mitochondria? What nucleic acids are found in mitochondria? What configuration of mitochondrial cristae corresponds to a low level of oxidative phosphorylation? Which mitochondrial membrane does contain mitochondrial porins and receptors for proteins and polypeptides translocating into the intermembrane space? Illustration of the cross section of a mitochondrion observed under different metabolic conditions. The condensed morphology appears in the presence of high ADP concentrations, when mitochondria are producing ATP (state III), while the orthodox configuration occurs at low ADP concentrations, with no production of ATP (state IV). https://doi.org/10.3390/membranes11070465  Where are the proteins contained in the membrane of peroxisomes synthesized? Where are the proteins contained in the lumen of the peroxisome synthesized? By TEM peroxisomes (P) generally show a matrix of moderate electron density. Aggregated electron-dense particles represent glycogen (G). X30,000. What are the functions of the peroxisome? What forms of peroxisome biogenesis exist in the cell? Which of the cell organelles universally contain catalase? What is the underlying cause of the various metabolic disorders associated with peroxisomes?  Micrograph showing microtubules (arrows) of the mitotic spindle in a dividing cell. On the right- microtubules are attached to the chromosomesx 30,000. Ross,Pawlina 2016. The apical part of an epithelial cell demonstrating intermediate filaments obtained using the quick-freeze deep-etch technique; TW - The terminal web of an epithelial cell IF – The intermediate filaments; R - The long, straight actin filament cores or rootlets, extending from the microvilli, cross-linked by a dense network of actin filaments containing numerous actin-binding proteins. The network of intermediate filaments can be seen beneath the terminal web anchoring the actin filaments of the microvilli. x47,000.  What do the minus/plus ends of microtubules and actin microfilaments mean? What is microtubule catastrophe? What proteins limit the polymerization of actin microfilaments? What proteins limit microtubule polymerization in MTOC? What is the microtubule - organizing center (MTOC)? How does MTOC work? What is the structure and function of MTOC? Which of the components of the cytoskeleton has no polarity? Which of the cytoskeletal components is associated with kinesin? What component of the cellular cytoskeleton consists of globular actin monomers linked into a double helix? What are the γ-tubulin rings within the MTOC (Microtubule Organizing Center)? Which cytoskeletal components is associated with kinesin? Which of the components of the cytoskeleton has no polarity? At the apical ends of the tall epithelial cells) are numerous very long stereocilia, which increase the surface area available for absorption.  Specializations of the Apical Cell Surface (c) TEM of microvilli sectioned longitudinally and transversely (inset) reveals the microfilament arrays that form the core of these projections. The terminal web (TW) of the cytoskeleton is also seen. G - The glycocalyx extending from glycoproteins and glycolipids of the microvilli plasmalemma contains certain enzymes for late stages of macromolecule digestion. TEM of cilia (C) sectioned longitudinally reveals the central X15,000. and peripheral microtubules of the axonemes. Cross sections (inset) clearly shows the 9 + 2 array of the microtubule doublets. At the base of each cilium is a basal body (B) anchoring the axoneme to the apical cytoplasm. Much shorter microvilli (MV) can be seen between the cilia. X59,000. Inset: X80,000.  This micrograph is taken from nerve tissue; Neurons contain both intermediate filaments and microtubules. Micrograph (a) shows an axon in transverse section wrapped in the cytoplasm of a Schwann cell. Intermediate filaments (known as neurofilaments in this case) are a prominent feature of nerve cells, providing internal support for the cell by cross-linkage with microtubules and other organelles. The neurofilaments NF are dispersed among and in parallel with the microtubules, but are much smaller in diameter. Micrograph (b) shows part of an axon in longitudinal section. The axonal microtubules provide structural support and transport along the axon.  A dorsal root ganglion. Satellite cells are very closely associated with cell bodies of sensory nerves and support these cells in various ways. X560. H&E These long-lived neurons commonly accumulate brown lipofuscin (L). S - satellite cells (S) surrounding ❖ Melanin is mainly responsible for skin color; is brown N - the perikarya of pigment; is also present in nerve cells in certain brain regions neurons such as the substantia nigra, shown in micrograph (b), where the cell cytoplasm is largely obscured by its content of brown melanin pigment. ▪ This specimen has been stained by the Azan method to pick out the nuclei N which are stained pale blue with prominent magenta nucleoli. What is characteristic of cell inclusions? (b) X30,000.Numerous individual or clustered electron-dense particles – glycogen granules in the liver cell cytoplasm, which lack membrane; form characteristic aggregates such as those shown; is a ready source of energy; are often abundant in cells with high metabolic activity.  White adipose tissue, human, H&E, x363; inset x700. The adipocytes (A) have a spherical profile in which they exhibit a very thin rim of cytoplasm surrounding a single, large fat-containing vacuole. Because the fat is lost during tissue preparation, one only sees the rim of cytoplasm and an almost clear space. Between the cells - delicate connective tissue stroma holding the adipocytes together, and within this stroma are small blood vessels (BV), mostly capillaries and venulesThe inset shows an adipocyte whose nucleus (N) is relatively easy to identify. It appears to reside within the rim of cytoplasm (Cy), giving (a) L - Lipid droplets in the cells of the adrenal cortex, have the adipocyte the classic “ signet ring” appearance. A second nucleus small spherical structures with homogenous matrices. (N’), partially out of the plane of section, appears to reside between the Are aggregates of hydrophobic lipid molecules cytoplasmic rims of two adjacent cells. Th is is probably the nucleus of a Are enclosed by fibroblast. Because of the relatively large size of the adipocyte, it is very ✔ a single monolayer of phospholipids infrequent that the nucleus of the cell is included in the plane of section ✔ with various peripheral proteins, of a given cell. Other cells that may be seen within the delicate ✔ including enzymes for lipid metabolism. connective tissue stroma are mast cells (MC). Pituitary neurosecretory axons of rats in PEG-TEM (Figure 2a) and conventional epoxy TEM (Figure 2b). Distinct strands with lower electron density form microtrabecular lattices (MTL) of strands (arrows) occupying the cytoplasmic matrix between membranous organelles including neurosecretory granules (g) and neurotubules and neurofilaments in PEG-TEM, while flocculent or fuzzy and ill-defined strands (arrows) are present in the cytoplasmic matrix in epoxy sections. Note well correspondence of strands between the two micrographs. Bar:0.1um. What are specific structures revealed by high-voltage electron microscopy within the cell cytosol? APOPTOSIS There are at least two broad signaling pathways that lead to apoptosis: ❖ The intrinsic pathway of apoptosis Begins when an injury occurs within the cell and the resulting stress activates the apoptotic pathway. Intrinsic stresses such as https://www.thermofisher.com/ge/en/home/life-science/antibodies/an tibodies-learning-center/antibodies-resource-library/cell-signaling-path - oncogenes, ways/cellular-apoptosis-pathway.html - direct DNA damage, - hypoxia, and - survival factor deprivation, can activate the intrinsic apoptotic pathway. p53 is - a sensor of cellular stress and - a critical activator of the intrinsic pathway (the p53 Pathway for Apoptosis Signaling). ❖ The extrinsic pathway of apoptosis. Begins outside a cell, when conditions in the extracellular environment determine that a cell must die. Based on the triggering stimulus and nature of the components involved, at least two apoptotic pathways can be differentiated: Schematic drawing of mechanisms leading to one involving receptor systems apoptosis. Both external and internal stimuli can one triggered by cytotoxic stress trigger apoptosis by activating the enzymatic caspase cascade. Many external activators act on the cell to initiate signals leading to apoptosis; note that ❖ In both the intrinsic and extrinsic pathway of apoptosis, signaling results: TNF and TGF-β act through a “death receptor.” In the activation of a family of Cys (Cysteine) proteases - caspases. Controlled release of cytochrome c and They act in a proteolytic cascade to dismantle and remove the dying cell. SMAC/DIABLO from mitochondria is an important internal step in the activation of apoptosis.  Cells undergoing apoptosis show the following biochemical features ❖ The Bcl-2 family Members They are central regulators of apoptosis, which either - inhibit or - promote caspase activation. A variety of signaling pathways regulate apoptosis by controlling the expression or activity of members of the Bcl-2 family. The BCL-2 family of proteins controls cell death primarily by direct binding interactions that regulate mitochondrial outer membrane permeability leading to - changes in the permeability of the mitochondrial membrane channels. - The integrity of the mitochondrion is breached. - The mitochondrial transmembrane potential drops, and - the electron-transport chain is disrupted. Proteins from the mitochondrial intermembrane space, such as o cytochrome c and o SMAC/DIABLO (second mitochondria-derived activator of caspases /direct inhibitor of apoptosis-binding protein with low isoelectric point [pI]) are released into the cytoplasm They activate a cascade of proteolytic enzymes - CASPASES responsible for dismantling the cell. They are ❖ They are the effectors of apoptosis Cleave more than 100 cellular proteins. Schematic drawing of mechanisms leading The irreversible release of intermembrane space proteins (cytochrome c, to apoptosis. Both external and internal SMAC/DIABLO) causes stimuli can trigger apoptosis by activating subsequent caspase activation and the enzymatic caspase cascade. Many external activators act on the cell to initiate apoptosis. signals leading to apoptosis; note that TNF The affinities and relative abundance of the BCL-2 family proteins dictate the and TGF-β act through a “death receptor.” predominate interactions between anti-apoptotic and pro-apoptotic BCL-2 family Controlled release of cytochrome c and proteins that regulate mitochondrial outer membrane permeability. SMAC/DIABLO from mitochondria is an important internal step in the activation of Changes in the permeability of the outer mitochondrial membrane causes loss of apoptosis. mitochondrial function.  Morphological features of cells undergoing apoptosis DNA fragmentation Occurs in the nucleus Is an irreversible event that commits the cell to die. DNA fragmentation is a result of Ca2+ - dependent and Mg2+ - dependent activation of nuclear endonucleases. These enzymes selectively cleave DNA, generating small oligonucleosomal fragments. Nuclear chromatin then aggregates The nucleus is divided into several discrete fragments bounded by the nuclear envelope. Decrease in cell volume Is achieved by shrinking of the cytoplasm. The cytoskeletal elements become reorganized in bundles parallel to the cell surface. Ribosomes become clumped within the cytoplasm The rER forms a series of concentric whorls Most of the endocytotic vesicles fuse with the plasma membrane. Membrane blebbing Results from cell membrane alterations. One alteration is related to translocation of certain molecules (e.g., phosphatidylserine) from the cytoplasmic surface to the outer surface of the plasma membrane. These changes cause the plasma membrane to change its physical and chemical properties and lead to blebbing without loss of membrane integrity Formation of apoptotic bodies Is the final step of apoptosis, results in cell breakage. These membrane-bounded vesicles originate from the cytoplasmic bleb containing organelles and nuclear material. They are quickly removed by phagocytic cells, and no inflammatory reaction occurs.  FIGURE 1. TEM of a necrotic cell: the disruption of plasma membrane and organelles is observable. A relative preservation of nuclear morphology appears. (original magnification: x 10,000) FIGURE 2 TEM of an apoptotic (A) and a normal (N) cell. The characteristic chromatin rearrangement appears in A, strongly different from its normal organization (N). The good preservation of membrane and organelles is also evident. (original magnification: x 8,000) FIGURE 3. SEM of a necrotic cell. Numerous lesions appear on the cell surface. (original magnification: x 5,000) FIGURE 4. SEM of an apoptotic cell. Surface blebbing is evident. (original magnification: x 5,000) FIGURE 5. FF freeze-fracture),of normal cell, nuclear envelope. The regular distribution of nuclear pores is visible. (original magnification: x 30,000) FIGURE 6. FF of apoptotic cell. The nuclear envelope shows a characteristic clustering (asterisc) of nuclear pores. (original magnification: x 35,000) APOPTOSIS vs. NECROSIS, M.Vitale, G.Zauli and E.Falcieri http://www.cyto.purdue.edu/cdroms/cyto4/15_apop/data/chap10.htm Damage to the plasma membrane of cells, rapid swelling and lysis of cells are characteristic signs of what type of cell death? What type of apoptosis is induced by a lack of cell-to-extracellular matrix interactions? ❖ What are morphological changes of cell undergoing apoptosis? ❖ What are biochemical changes of cells undergoing apoptosis? ❖ What is characteristic for What are effector proteins of apoptosis? DNA fragmentation What are regulators of apoptosis? Decrease in cell volume What are the differences between What is characteristic of necrosis? intrinsic and extrinsic pathway of apoptosis? Loss of mitochondrial What is characteristic of apoptosis? function What is characteristic of entosis? Membrane blebbing What is characteristic of necroptosis? Formation of apoptotic What type of cell death is caused by bodies infection with some microorganisms that cause intense inflammatory reactions? The End.