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.

中文翻译：

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果蝇唾液腺内陷的三维顶点模型。

在上皮形态发生过程中，在细胞水平上产生的力不仅引起细胞变形，而且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，我们使用一种新颖的三维顶点模型来探索果蝇胚胎唾液腺形成过程中细胞力的作用。将斑块表示为最初的柱状细胞的上皮层，我们关注由于三个放线菌素池而引起的收缩力的时空分布：斑块坑中的apicomedial放线菌素，坑外的连接性放线菌素弧和超细胞上的放线菌素电缆沿着基板的圆周。在计算机模拟“野生型”模型中，根据实验数据，这些池在不同的时间被激活。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硅“突变体”，其中仅一个或两个肌球蛋白池被激活。我们发现apicomedial肌球蛋白在凹坑中会引发一个小酒窝，但这对于基板的整体内陷不是必需的。肌球蛋白弧是内翻的主要驱动力，并负责根尖表面的内在化。周向肌动球蛋白电缆起收缩显影管开口的作用，并负责形成适当形状的内腔。细胞插层倾向于促进内陷，但是我们模型的几何约束仅允许少量插层，其作用很小。该模型预测的斑块内陷与实验观察结果基本一致。