Here we describe for the first time the kinetics how the maturation of filopodia shaft adhesions correlates with the cyclic protrusion and retraction activities of the lamellipodium. While filopodia adhesions were previously found to be integrated into the cell lamella of various cell types, no information was available about the integration process. Here we show that filopodia shaft adhesions grow and mature in sequential phases that correlate with the advancing and pausing of the adjacent lamellipodium. We also show that vinculin gets recruited into the filopodia shaft adhesions, which suggests that they are exposed to tensile forces. In contrast to the previously described behavior of nascent adhesions within lamellipodia, which remain point-like and can be turnedover rapidly, the b3-integrin-rich filopodia shaft adhesions once formed increase rapidly in length and their initial formation typically induces the advancement of the Betamethasone Dipropionate proximal lamellipodium. In the next phase, the rearward growing filopodia shaft adhesions are overrun by the advancing lamellipodium until the point, where the lamellipodia pauses at the distal edges of filopodia shaft adhesions. Once lamellipodia started to pause, the now integrated filopodia shaft adhesions started to grow in width. Previous studies have shown that the activity of myosin II just behind the lamellipodium-lamellum transition zone regulate the cyclic retraction of the lamellipodium and the maturation of cell-matrix adhesions and substrate rigidity sensing. Our work could show now that the maturation of filopodia adhesions and their integration into the lamellum are also regulated by tensile forces. This was suggested by the upregulated recruitment of vinculin, which only binds to stretched but not relaxed talin, and the temporal increase of integrin fluorescence in filopodia shaft adhesions once reached by the advancing lamellipodium, and by the existence of the cyclic protrusions and retractions of lamellipodia in the proximity of filopodia adhesions on FN-coated rigid and soft surfaces. MLCK Nitrendipine inhibition blocked the periodic protrusions and retractions of the lamellipodium as previously described.