Typically filopodia are quite dynamic and are constantly growing or retracting. Thus, periods of stasis are often short-lived and even adhesion of the filopodial tip to a substrate will not last long before the cell pulls on the site and recruits additional components or retracts, leaving behind a thin tube of membrane. There are several events that may promote stasis in retracting filopodia.
1) Ligand binding to filopodial receptors and subsequent adhesion of the ligand/receptor complex to actin bundles:
After a ligand binds to a receptor on the filopodium, lateral connections between the receptor and the actin bundle(s) prevent retrograde actin movement relative to the ligand. This inhibition converts the previous retrograde movement of the retracting filaments into tension on the bundles. This tension might influence polymerization and stability of actin filaments and/or myosin activity.
2) Ligand binding to filopodial receptors followed by uncapping of filament barbed ends:
Retracting filopodia become static when receptor binding leads to filament uncapping and rapid polymerization at the barbed end. The retraction force is converted to retrograde flux and the filament length remains constant.
3) Capping of unstable actin filaments:
If retraction occurs by barbed end disassembly, capping of unstable filaments by an activated receptor will block retraction and induce stasis .