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顶端收缩需要有模式的顶端表面重塑来同步细胞变形。

Apical constriction requires patterned apical surface remodeling to synchronize cellular deformation.

作者信息

Yamashita Satoshi, Ishihara Shuji, Graner François

机构信息

Laboratory for Morphogenetic Signaling, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan.

Graduate School of Arts and Sciences, The University of Tokyo, Tokyo, Japan.

出版信息

Elife. 2025 Apr 17;13:RP93496. doi: 10.7554/eLife.93496.

Abstract

Apical constriction is a basic mechanism for epithelial morphogenesis, making columnar cells into wedge shape and bending a flat cell sheet. It has long been thought that an apically localized myosin generates a contractile force and drives the cell deformation. However, when we tested the increased apical surface contractility in a cellular Potts model simulation, the constriction increased pressure inside the cell and pushed its lateral surface outward, making the cells adopt a drop shape instead of the expected wedge shape. To keep the lateral surface straight, we considered an alternative model in which the cell shape was determined by cell membrane elasticity and endocytosis, and the increased pressure is balanced among the cells. The cellular Potts model simulation succeeded in reproducing the apical constriction, and it also suggested that a too strong apical surface tension might prevent the tissue invagination.

摘要

顶端收缩是上皮细胞形态发生的一种基本机制,它使柱状细胞变成楔形,并使扁平的细胞片弯曲。长期以来,人们一直认为顶端定位的肌球蛋白会产生收缩力并驱动细胞变形。然而,当我们在细胞Potts模型模拟中测试增加的顶端表面收缩力时,收缩增加了细胞内的压力,并将其侧面推向外,使细胞呈现出液滴形状,而不是预期的楔形。为了保持侧面笔直,我们考虑了另一种模型,其中细胞形状由细胞膜弹性和内吞作用决定,增加的压力在细胞间得到平衡。细胞Potts模型模拟成功地再现了顶端收缩,并且还表明过强的顶端表面张力可能会阻止组织内陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9942/12005724/1a3b888b3e96/elife-93496-fig1.jpg

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