Remodeling the zonula adherens in response to tension and the role of afadin in this response.
Remodeling the zonula adherens in response to tension and the role of afadin in this response.
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DOI：
10.1083/jcb.201506115
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发表时间：
2016-04-25
期刊：
影响因子：
--
通讯作者：
Peifer M
中科院分区：
文献类型：
--
作者：
Choi W;Acharya BR;Peyret G;Fardin MA;Mège RM;Ladoux B;Yap AS;Fanning AS;Peifer M
在发育过程中，上皮细胞必须在不破坏上皮屏障功能的情况下产生张力并对张力作出反应。作者在MDCK细胞中使用超分辨率显微镜检查粘附小带（ZA）如何在保持组织完整性的同时对收缩性升高作出反应。他们定义了封闭小带家族蛋白在调节收缩性和支架蛋白afadin在维持三细胞连接处ZA结构中的关键作用。形态发生需要细胞-细胞粘附和细胞骨架之间的动态协调，以允许细胞改变形状和移动而不失去组织完整性。我们在一个简单的模型上皮细胞系中使用遗传工具和超分辨率显微镜来定义细胞-细胞粘附小带（ZA）的分子结构如何响应收缩性升高而被修改，以及这些细胞如何保持组织完整性。我们以前发现，耗尽封闭小带1（ZO-1）家族蛋白在MDCK细胞诱导高度组织化的收缩肌动球蛋白阵列在ZA。我们发现，ZO敲低通过Shroom3/Rho相关的卷曲螺旋蛋白激酶（ROCK）途径提高收缩力。我们的数据表明，每个双细胞边界是一个独立的收缩单位，与肌动蛋白电缆锚定端上的钙粘蛋白复合物在三细胞交界处。细胞通过增加连接的afadin来响应升高的收缩性。虽然ZO/afadin敲低并不能阻止收缩阵列组装，但它显著改变了细胞形状和屏障功能，以响应收缩性升高。我们建议，afadin作为一个强大的蛋白质支架，保持ZA架构在三细胞连接。
During development, epithelial cells must generate and respond to tension without disrupting epithelial barrier function. The authors use superresolution microscopy in MDCK cells to examine how the zonula adherens (ZA) is remodeled in response to elevated contractility while maintain tissue integrity. They define key roles for zonula occludens family proteins in regulating contractility and for the scaffolding protein afadin in maintaining ZA architecture at tricellular junctions. Morphogenesis requires dynamic coordination between cell–cell adhesion and the cytoskeleton to allow cells to change shape and move without losing tissue integrity. We used genetic tools and superresolution microscopy in a simple model epithelial cell line to define how the molecular architecture of cell–cell zonula adherens (ZA) is modified in response to elevated contractility, and how these cells maintain tissue integrity. We previously found that depleting zonula occludens 1 (ZO-1) family proteins in MDCK cells induces a highly organized contractile actomyosin array at the ZA. We find that ZO knockdown elevates contractility via a Shroom3/Rho-associated, coiled-coil containing protein kinase (ROCK) pathway. Our data suggest that each bicellular border is an independent contractile unit, with actin cables anchored end-on to cadherin complexes at tricellular junctions. Cells respond to elevated contractility by increasing junctional afadin. Although ZO/afadin knockdown did not prevent contractile array assembly, it dramatically altered cell shape and barrier function in response to elevated contractility. We propose that afadin acts as a robust protein scaffold that maintains ZA architecture at tricellular junctions.
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影响因子：
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DOI：
10.1083/jcb.201309092
发表时间：
2014-04-28
期刊：
The Journal of cell biology
影响因子：
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发表时间：
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期刊：
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