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非中心体微管和 II 型肌球蛋白增强表皮细胞黏附和屏障形成。

Noncentrosomal microtubules and type II myosins potentiate epidermal cell adhesion and barrier formation.

机构信息

Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.

出版信息

J Cell Biol. 2012 Oct 29;199(3):513-25. doi: 10.1083/jcb.201206143. Epub 2012 Oct 22.

Abstract

During differentiation, many cells reorganize their microtubule cytoskeleton into noncentrosomal arrays. Although these microtubules are likely organized to meet the physiological roles of their tissues, their functions in most cell types remain unexplored. In the epidermis, differentiation induces the reorganization of microtubules to cell-cell junctions in a desmosome-dependent manner. Here, we recapitulate the reorganization of microtubules in cultured epidermal cells. Using this reorganization assay, we show that cortical microtubules recruit myosin II to the cell cortex in order to engage adherens junctions, resulting in an increase in mechanical integrity of the cell sheets. Cortical microtubules and engaged adherens junctions, in turn, increase tight junction function. In vivo, disruption of microtubules or loss of myosin IIA and B resulted in loss of tight junction-mediated barrier activity. We propose that noncentrosomal microtubules act through myosin II recruitment to potentiate cell adhesion in the differentiating epidermis, thus forming a robust mechanical and chemical barrier against the external environment.

摘要

在分化过程中,许多细胞将其微管细胞骨架重新组织成非中心体的阵列。尽管这些微管可能是为了满足其组织的生理作用而组织起来的,但它们在大多数细胞类型中的功能仍未被探索。在表皮中,分化诱导微管以依赖于桥粒的方式重新组织到细胞-细胞连接处。在这里,我们重现了培养表皮细胞中微管的重排。使用这种重排测定,我们表明皮质微管将肌球蛋白 II 募集到细胞皮质,以参与黏着连接,从而增加细胞片层的机械完整性。皮质微管和参与的黏着连接反过来又增加了紧密连接的功能。在体内,微管的破坏或肌球蛋白 IIA 和 IIB 的缺失导致紧密连接介导的屏障活性丧失。我们提出,非中心体微管通过肌球蛋白 II 的募集来增强分化表皮中的细胞黏附,从而形成一个强大的机械和化学屏障,以抵御外部环境。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ca1/3483132/b83d637f1c3f/JCB_201206143_Fig1.jpg

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