Myosin II controls junction fluctuations to guide epithelial tissue ordering
Myosin II controls junction fluctuations to guide epithelial tissue ordering
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肌球蛋白 II 控制连接波动以指导上皮组织排序
DOI：
10.1101/078204
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Curran S
中科院分区：
文献类型：
--
作者：
Curran S
在稳态条件下，单个粘附连接（AJs）长度的动态变化为上皮细胞提供了在面对内在和外在力量时维持组织完整性所需的流动性。虽然AJ重塑对发育形态发生的贡献已被深入研究，但对其他情况下AJ动力学的了解较少。在这里，我们研究了上皮中的AJ动力学，该上皮经历了逐渐增加的包装顺序，而没有伴随组织大小或形状的大规模变化。我们发现相邻交换事件是由连接长度的随机波动驱动的，部分由连接肌动球蛋白调节。在这种情况下，各向同性连接肌动球蛋白的发育增加降低了邻居交换的速度，有助于组织秩序。我们提出了一个模型，在该模型中，结点之间张力的局部变化决定了基于肌动球蛋白的力是否会抑制或驱动拓扑转变，从而改善或变形组织。
Under conditions of homeostasis, dynamic changes in the length of individual adherens junctions (AJs) provide epithelia with the fluidity required to maintain tissue integrity in the face of intrinsic and extrinsic forces. While the contribution of AJ remodeling to developmental morphogenesis has been intensively studied, less is known about AJ dynamics in other circumstances. Here, we study AJ dynamics in an epithelium that undergoes a gradual increase in packing order, without concomitant large-scale changes in tissue size or shape. We find that neighbor exchange events are driven by stochastic fluctuations in junction length, regulated in part by junctional actomyosin. In this context, the developmental increase of isotropic junctional actomyosin reduces the rate of neighbor exchange, contributing to tissue order. We propose a model in which the local variance in tension between junctions determines whether actomyosin-based forces will inhibit or drive the topological transitions that either refine or deform a tissue.