Similarly, inclination and length at the back are controlled by the depolymerization rate. In the simulations, coronin is localized at the top and covers the back of the actin waves. However, it is not most concentrated at the roof of the actin network, but appears to slightly lag F-actin localization with peak density relatively close to that of F-actin, as shown in Figure 12. Simulation shows that inhibition of coronin leads to actin waves with increased height and possibly alters the entire actin structure with sufficiently unbalanced branching dynamics. Alternate Factin structures, including triggering waves and an expanding dome-like structure, may be induced by reduced coronin debranching activity, as depicted in Figure 13. These structures are similar to gelation actin waves that are caused by reduction in the effective debranching rate, observed in. To study whether coronin specificity for F-actin has a role in determination of the shape of actin waves, we performed simulations on a system without coronin. It appears that coronin is not explicitly required for formation of the traveling waves as long as filament deconstruction is sufficiently compensated by spontaneous debranching. In reality, other mechanisms such as filament severing and rapid filament disintegration could account for additional filament deconstruction. To simulate PTEN activity, we locally disable Rac activation. When we add the PTEN activity to a fixed region, an actin wave cannot propagate Ginsenoside-Ro through the region. Instead, its propagation is blocked near the border and the wave front becomes a standing wave. If the PTEN Diperodon region pushes into the area covered by the actin wave, the wave front propagates backward as the covered area shrinks. Figures 15 displays the dynamics of a retracting wave front due to PTEN progression, and Figure 16 shows the F-actin structure of the retracting actin wave at t~35s. Since the peak in F-actin density is determined by the balance between available network components and the activity of activated WASP, the former of which is high outside and the latter high inside the enclosed region, receding fronts of actin waves should be present, and indeed observed, in the same fashion as the expanding fronts. A close examination of coronin localization shows that coronin trails the wave front, in this case appearing outside the enclosed area, in good agreement with experimental observations. Finally, we study PTEN ingression into an area covered by actin waves and separation of actin waves caused by a broken wave front. Figure 17 depicts the experimentally-observed PTEN ingression and separated actin waves, and simulations of the actin network in a vertical cross-section noted by white lines. For PTEN ingression, wave fronts along the cross-section retreat as the PTEN-covered area expands, in good agreement with the observations. For separated actin waves, a broken wave front leads to formation of new wave fronts which eventually connect with existing wave fronts and separate the wave-surrounded region. Although data on PTEN localization is not available for separation of actin waves, simulated F-actin density along the vertical cross-section when PTEN intrudes at the middle of the covered region agrees well with the experimental observations. Figure S1 displays the dynamics of new wave-front formation. Simulation suggests that introduction of the PTEN activity inhibits the positive feedback through PIP3 in this area, leading to eradication of the actin structure. New wave fronts are subsequently formed at the border of the region, separating the former area into two enclosed areas.