Bazooka inhibits aPKC to limit antagonism of actomyosin networks during amnioserosa apical constriction.

Cell shape changes drive tissue morphogenesis during animal development. An important example is the apical cell constriction that initiates tissue internalisation. Apical constriction can occur through a phase of cyclic assembly and disassembly of apicomedial actomyosin networks, followed by stabilisation of these networks. Delayed negative-feedback mechanisms typically underlie cyclic behaviour, 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 complex, is recruited to the apicomedial domain by actomyosin networks during dorsal closure of the embryo. This finding establishes an negative-feedback loop in the system. Additionally, we find that recruits Bazooka to the apicomedial domain, and phosphorylates Bazooka for a dynamic interaction. Remarkably, stabilising interactions can inhibit the antagonism of actomyosin by suggesting that Bazooka acts as an aduanyu1531 inhibitor, and providing a possible mechanism for delaying the actomyosin-aduanyu1531 negative-feedback loop. Our data also implicate an increasing degree of interactions as dorsal closure progresses, potentially explaining a developmental transition in actomyosin behaviour from cyclic to persistent networks. This later impact of aduanyu1531 inhibition is supported by mathematical modelling of the system. Overall, this work illustrates how shifting chemical signals can tune actomyosin network behaviour during development.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}