Dorsal closure is a morphogenetic process in Drosophila embryogenesis, whereby an epidermis opening closes. The epidermal opening is filled with the Amnioserosa (AS) tissue, which drives dorsal closure by apical constriction of its individual cells. Apical constriction in turn is driven by apical surface area oscillations of AS cells, which are the result of periodically forming, transient actomyosin foci. It is currently unclear whether neighboring cells coordinate their oscillations and how the cell scale behavior leads to tissue scale dynamics. To better understand these aspects, we developed a coupled finite element simulation of actomyosin dynamics, force generation, and material behavior. Thereby, we model the dynamics of the actomyosin network in AS cells with reaction-diffusion equations at the subcellular level in 2D. The actomyosin concentration determines the strength of local contractions within the AS cell surfaces. Based on our in vivo observations, we model the dynamics of actin binding proteins (eg. Arp2/3) as an activator-depleted substrate system, and couple it to actin network formation. Analytical methods describe the system behavior in the absence of mechanical deformation, and predict how the system will evolve in coupled simulations. We model the surrounding epidermis as a linear viscoelastic material, so that it adapts in response to the pulling force of the AS tissue, as shown experimentally. Our simulations reproduce dorsal closure and make clear predictions that ask for experimental testing. In particular, a sequential arrest of cellular oscillations simply emerges, similar to what was observed in vivo. So far, a dpp-signaling gradient was thought to control this phenomenon. Addressing this experimentally provides support for the model prediction. Interestingly, 3D finite element simulations predict that the emerging sequential pulsation arrest generates a contractility gradient, which controls AS tissue morphogenesis.