During tissue morphogenesis, the changes in cell shape, resulting from cell-generated forces, often require active regulation of intracellular trafficking. How mechanical stimuli influence intracellular trafficking and how such regulation impacts tissue mechanics are not fully understood. In this study, we identify an actomyosin-dependent mechanism involving Rab11-mediated trafficking in regulating apical constriction in the Drosophila embryo. During Drosophila mesoderm invagination, apical actin and Myosin II (actomyosin) contractility induces apical accumulation of Rab11-marked vesicle-like structures (“Rab11 vesicles”) by promoting a directional bias in dynein-mediated vesicle transport. At the apical domain, Rab11 vesicles are enriched near the adherens junctions (AJs). The apical accumulation of Rab11 vesicles is essential to prevent fragmented apical AJs, breaks in the supracellular actomyosin network, and a reduction in the apical constriction rate. This Rab11 function is separate from its role in promoting apical Myosin II accumulation. These findings suggest a feedback mechanism between actomyosin activity and Rab11-mediated intracellular trafficking that regulates the force generation machinery during tissue folding.

中文翻译：

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Rab11 囊泡的肌动球蛋白活性依赖性顶端靶向增强顶端收缩

在组织形态发生过程中，由细胞产生的力引起的细胞形状的变化通常需要主动调节细胞内运输。机械刺激如何影响细胞内运输以及这种调节如何影响组织力学尚不完全清楚。在这项研究中，我们确定了一种肌动球蛋白依赖性机制，涉及 Rab11 介导的运输来调节果蝇胚胎的顶端收缩。在果蝇中胚层内陷期间，顶端肌动蛋白和肌球蛋白 II（肌动球蛋白）收缩性通过促进动力蛋白介导的囊泡运输的方向性偏差，诱导 Rab11 标记的囊泡样结构（“Rab11 囊泡”）在顶端积累。在顶端区域，Rab11 囊泡在粘附连接 (AJ) 附近富集。 Rab11 囊泡的顶端积累对于防止顶端 AJ 碎片、细胞上肌动球蛋白网络断裂以及顶端收缩率降低至关重要。 Rab11 的这种功能与其促进顶端肌球蛋白 II 积累的作用是分开的。这些发现表明肌动球蛋白活性和 Rab11 介导的细胞内运输之间存在反馈机制，可调节组织折叠过程中的力产生机制。