During epithelial morphogenesis, force generation at the cellular level not only causes cell deformation, but may also produce coordinated cell movement and rearrangement on the tissue level. In this paper, we use a novel three-dimensional vertex model to explore the roles of cellular forces during the formation of the salivary gland in the Drosophila embryo. Representing the placode as an epithelial sheet of initially columnar cells, we focus on the spatial and temporal patterning of contractile forces due to three actomyosin pools: the apicomedial actomyosin in the pit of the placode, junctional actomyosin arcs outside the pit, and a supracellular actomyosin cable along the circumference of the placode. In an in silico ‘wild type’ model, these pools are activated at different times according to experimental data. To identify the role of each myosin pool, we have also simulated various in silico ‘mutants’ in which only one or two of the myosin pools are activated. We find that the apicomedial myosin initiates a small dimple in the pit, but this is not essential for the overall invagination of the placode. The myosin arcs are the main driver of invagination and are responsible for the internalization of the apical surface. The circumferential actomyosin cable acts to constrict the opening of the developing tube, and is responsible for forming a properly shaped lumen. Cell intercalation tends to facilitate the invagination, but the geometric constraints of our model only allow a small number of intercalations, and their effect is minor. The placode invagination predicted by the model is in general agreement with experimental observations. It confirms some features of the current ‘belt-and-braces’ model for the process, and provides new insights on the separate roles of the various myosin pools and their spatio-temporal coordination.

在上皮形态发生过程中，细胞水平的力产生不仅会导致细胞变形，还可能在组织水平上产生协调的细胞运动和重排。在本文中，我们使用一种新的三维顶点模型来探索细胞力在果蝇胚胎唾液腺形成过程中的作用。将基板表示为最初柱状细胞的上皮片，我们专注于由三个肌动球蛋白池引起的收缩力的空间和时间模式：基板凹坑中的顶端肌动球蛋白、凹坑外的连接肌动球蛋白弧和细胞上肌动球蛋白沿着基板圆周的电缆。在硅片中在“野生型”模型中，这些池根据实验数据在不同时间被激活。为了确定每个肌球蛋白池的作用，我们还模拟了各种计算机“突变体”，其中只有一个或两个肌球蛋白池被激活。我们发现顶端肌球蛋白在凹坑中形成一个小酒窝，但这对于基板的整体内陷并不是必不可少的。肌球蛋白弧是内陷的主要驱动力，负责顶端表面的内化。圆周肌动球蛋白缆线的作用是收缩发育管的开口，并负责形成适当形状的管腔。细胞嵌入倾向于促进内陷，但我们模型的几何约束只允许少量嵌入，并且它们的影响很小。该模型预测的基板内陷与实验观察大体一致。它确认了当前流程的“腰带和支架”模型的一些特征，