In: Biology
The locomotion of fibroblasts in culture is immediately halted by the drug cytochalasin, whereas colchicine causes fibroblast to cease to move directionally and to begin extending lamellipodia in seemingly random directions.inkection of anti-vimentin has no obvious effect on fibroblast migration.what do these results suggest about the role of the cytoskeleton in fibroblast movement?
Cytochalasin is a drug which inhibits polymerisation of the actin filament. G-actins with ATP bound form are continuously added to the + end of the actin filament. This causes increase in the actin length. Cytochalasin hydrolyses ATP into ADP. G-actins with ADP bound form in unable to increase length. Like this way cytochalasin inhibits actin polymerization.
Actins have immense roles to play in the movement of fibroblast cells. New actin filaments are formed towards the end of leading edge of the moving cells. As polymerisation of actins is inhibited thus cytochalasin treated cells are unable to move.
Colchicine is a drug used to inhibit the polymerization of microtubules but doesn't inhibit polymerization of actin filaments. Colchicine treated cells extend lamellipodia to all directions. Thus it is clear that colchicine treatment does not inhibit lamellipodia extension. So, actin filaments are necessary for formation of lamellipodia extensions during cell movement. But microtubules are necessary for movement of cells towards a specific direction.
Vimentin is a type of intermediate filament. Anti-vimentin treatment doesn't hamper cell movement. This clears that intermediate filaments don't have any role in cell movement.