Tissue remodelling during Drosophila embryogenesis is notably driven by epithelial cell contractility. This behaviour arises from the Rho1–Rok-induced pulsatile accumulation of non-muscle myosin II pulling on actin filaments of the medioapical cortex. While recent studies have highlighted the mechanisms governing the emergence of Rho1–Rok–myosin II pulsatility, little is known about how F-actin organization influences this process. Here, we show that the medioapical cortex consists of two entangled F-actin subpopulations. One exhibits pulsatile dynamics of actin polymerization in a Rho1-dependent manner. The other forms a persistent and homogeneous network independent of Rho1. We identify the formin Frl (also known as Fmnl) as a critical nucleator of the persistent network, since modulating its level in mutants or by overexpression decreases or increases the network density. Absence of this network yields sparse connectivity affecting the homogeneous force transmission to the cell boundaries. This reduces the propagation range of contractile forces and results in tissue-scale morphogenetic defects.

果蝇过程中的组织重塑胚胎发生明显受到上皮细胞收缩力的驱动。此行为是由Rho1-Rok诱导的非肌肉肌球蛋白II的搏动性蓄积拉动了中尖顶皮层的肌动蛋白丝引起的。尽管最近的研究强调了控制Rho1-Rok-肌球蛋白II搏动发生的机制，但对F-肌动蛋白组织如何影响这一过程的了解很少。在这里，我们显示了中尖顶皮层由两个纠缠的F-肌动蛋白亚群组成。一个以Rho1依赖的方式展现肌动蛋白聚合的搏动动力学。另一个形成独立于Rho1的持久性同质网络。我们将formin Frl（也称为Fmnl）确定为持久性网络的关键成核剂，因为在突变体中或通过过度表达调节其水平会降低或增加网络密度。缺少此网络会产生稀疏的连接性，从而影响均匀力向细胞边界的传递。这减小了收缩力的传播范围，并导致组织规模的形态发生缺陷。