Abstract - Cell shape changes drive tissue morphogenesis during animal development. An important example is apical cell constriction that initiates tissue internalization. Apical constriction can occur through a phase of cyclic assembly and disassembly of apicomedial actomyosin networks, followed by stabilization of these networks. Delayed negative feedback mechanisms typically underlie cyclic behavior, but the mechanisms regulating cyclic actomyosin networks remain obscure, as do mechanisms that transform overall network behaviour. Here, we show that a known inhibitor of apicomedial actomyosin networks in Drosophila amnioserosa cells, the Par-6-aPKC complex, is recruited to the apicomedial domain by actomyosin networks during dorsal closure of the embryo. This finding establishes an actomyosin-aPKC negative feedback loop in the system. Additionally, we find that aPKC recruits Bazooka/Par-3 to the apicomedial domain, and phosphorylates Bazooka for a dynamic interaction. Remarkably, stabilizing aPKC-Bazooka interactions can inhibit the antagonism of actomyosin by aPKC, suggesting Bazooka acts as an aPKC inhibitor, and providing a possible mechanism for delaying the actomyosin-aPKC negative feedback loop. Our data also implicate an increasing degree of Par-6-aPKC-Bazooka interactions as dorsal closure progresses, potentially explaining a developmental transition in actomyosin behavior from cyclic to persistent networks. This later impact of aPKC inhibition is supported by mathematical modeling of the system. Overall, this work illustrates how shifting chemical signals can tune actomyosin network behavior during development.