BIOL3S0 CELL BIOLOGY TAKE-HOME 2 (100pts) Spring 2018 6. PSr2 06 described exper
ID: 213438 • Letter: B
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BIOL3S0 CELL BIOLOGY TAKE-HOME 2 (100pts) Spring 2018 6. PSr2 06 described experiments to test the eftect of Cylochaiasin B Pease aw efer back to PS#2 Q6 for details and results ) Suppose you perform a similar expenment ta decorating actin microfiaments with myosin heads. A. (8pts) Please ncubation in the absence or draw the expected way the actin microflaments wil look at different smes athe presence of Cylochalasin B. (Circles represent actin monomers) -cytochalasin B Before adding Added monomers for short ime Added monomers For long time B (4pts) What is the strongest conclusion you couls make about the effects of on actin growth from the results you drew in Pat A? 7. (10pts) Please describe the molecular processes by which a neutrophil senses, poiarizes and crawls in the right direction to move towards pathogens Your response should include Arp 2/3 ChemotractantN-WASP Myosin Focal adhosion ATP hydrolysis Pushing forceExplanation / Answer
Q.7 Ans.- Chemotaxis—the directed movement of cells in a gradient of chemoattractant—is essential for neutrophils to crawl to sites of inflammation and infection and for Dictyostelium discoideum (D. discoideum) to aggregate during morphogenesis. Chemoattractant-induced activation of spatially localized cellular signals causes cells to polarize and move toward the highest concentration of the chemoattractant. Extensive studies have been devoted to achieving a better understanding of the mechanism(s) used by a neutrophil to choose its direction of polarity and to crawl effectively in response to chemoattractant gradients. Recent technological advances are beginning to reveal many fascinating details of the intracellular signaling components that spatially direct the cytoskeleton of neutrophils and D. discoideum and the complementary mechanisms that make the cell's front distinct from its back.Neutrophils respond to stimulation of chemoattractants by quickly establishing a leading edge (pseudopod), which protrudes toward the source of the chemoattractant. This chemoattractant-triggered symmetry breaking first requires the receptors on the cell surface to transmit a signal from the extracellular ligand to the cell interior. The next step is gradient interpretation, during which the cell must identify the portion of its surface that receives the greatest external signal. This interpretation requires a mechanism of comparing signaling levels throughout the cell surface and restricting leading-edge activity to the most highly stimulated region. This mechanism has been referred to as the “compass” mechanism because of its ability to spatially direct actin polymerization to the pseudopod of protruding neutrophil. The final component of chemotaxis is the stimulation of the regulators of actin polymerization, leading to the accumulation of actin polymers at the leading edge. HS1 is a contractin homolog, however its role in neutrophil chemotaxis is not known. HS1 interacts with Arp 2/3 , regulates Vav1 and Rac siglaning , and is necessary for efficient neutrophi chemotaxis. extracellular adenosine triphosphate present in thermally injured tissue, modulates the inflammatory response and causes significant tissue damage. the authors hypothesize that neutrophil infiltration and ensuing tissue necrosis would be mitigated by removing ATP-dependent siglaning at the burn site. Cdc42 regulates neutrophil migration via crosstalk between WASp, CD11b and microtubules. Neutrophil capture and recruitment from the circulation requires the formation of specific receptors/ligand bonds under hydrodynamic forces. In the present study we examine bond formation between integrins on neutrophils and immobilized ICAM-1 while using micropipettes to control force of contact between cell and substrate. Magnesium was used to induce to high effinity conformation of the integrins, and bond formation was assessed by measuring the probability of adhesion during repeated contacts. increasing the impingement force caused an increase in contact area and lead to a proportional increase in adhesion probability over the range of forces tested . in addition, different sized beads were used to change the force per unit area in the contact zone. We conclude that for a given contact stress, the rate of bond formation increases linearly with contact area, but that increasing contact stress results in higher intrinsic rates of bond formation.
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