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Cell-matrix adhesion and cell-cell adhesion differentially control basal myosin oscillation and Drosophila egg chamber elongation

机译:细胞基质黏附和细胞黏附差异控制基底肌球蛋白振荡和果蝇卵腔伸长

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Pulsatile actomyosin contractility, important in tissue morphogenesis, has been studied mainly in apical but less in basal domains. Basal myosin oscillation underlying egg chamber elongation is regulated by both cell–matrix and cell–cell adhesions. However, the mechanism by which these two adhesions govern basal myosin oscillation and tissue elongation is unknown. Here we demonstrate that cell–matrix adhesion positively regulates basal junctional Rho1 activity and medio-basal ROCK and myosin activities, thus strongly controlling tissue elongation. Differently, cell–cell adhesion governs basal myosin oscillation through controlling medio-basal distributions of both ROCK and myosin signals, which are related to the spatial limitations of cell–matrix adhesion and stress fibres. Contrary to cell–matrix adhesion, cell–cell adhesion weakly affects tissue elongation. In vivo optogenetic protein inhibition spatiotemporally confirms the different effects of these two adhesions on basal myosin oscillation. This study highlights the activity and distribution controls of basal myosin contractility mediated by cell–matrix and cell–cell adhesions, respectively, during tissue morphogenesis.
机译:在组织形态发生中起重要作用的搏动性肌动球蛋白收缩力,主要在根尖进行了研究,而在基底域则较少。卵室延伸的基础肌球蛋白振荡受细胞基质和细胞间粘附的调节。但是,这两种粘附控制基底肌球蛋白振荡和组织伸长的机制尚不清楚。在这里,我们证明细胞与基质的粘附可正向调节基底连接Rho1活性以及中基底ROCK和肌球蛋白的活性,从而强烈地控制组织的伸长。不同的是,细胞间粘附通过控制ROCK和肌球蛋白信号的中基底分布控制基底肌球蛋白的振荡,这与细胞基质粘附和应力纤维的空间限制有关。与细胞-基质粘附相反,细胞-细胞粘附对组织伸长的影响很小。体内光遗传学蛋白抑制时空证实了这两种粘附对基础肌球蛋白振荡的不同影响。这项研究强调了组织形态发生过程中,分别由细胞基质和细胞间粘附介导的基础肌球蛋白收缩活动和分布控制。

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