You are interested in the detailed effects of cytochalasin D on microfilaments over time. Based on what you know about the molec
ular mechanism of action of cytochalasins, describe what happens to MFs in cells treated with the drug. In particular, explain why existing actin polymers eventually depolymerize.
Basically Cytochalasin D inhibits the rate of actin polymerization and how actin filaments interacts with its barbed end in solution.
It does this byinhibiting the addition of more actin monomers to the 'barbed' or 'unsealed' end of the filaments meant for rapid addition of monomers.On binding,it blocked or capped the barbed end of the actin filaments inhibiting,monomers addition and polymerization.
Thus the failure of addition of more monomers inhibits polymerization and prevent elongation of actin filaments. Generally,Cytochalasin inhibits polymerisation at low concentration .Thus at low concentration of 2uM its inhibits actin polymerization by 90%.
Actin depolymerizing factor binds F-actin cooperatively and induces a conformational change in F-actin that causes it to twist further and become more destabilized. This twisting causes severing of the bond between actin monomers, depolymerizing the filament.
Explanation:
Actin filament depolymerization ensures the turnover of actin filaments within these structures and maintains a pool of actin monomers that permits the continual restructuring and growth of the actin cytoskeleton. ADF/cofilin influences actin filament turnover.
I believe the correct answer among the choices listed above is option A. Cars entering our field of vision from the side require the use of peripheral vision. This is the side vision. The vision that occurs outside the very center of gaze. Hope this answers the question.
