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光谱斑联蛋白短停蛋白是一种参与上皮闭合的重要微管调节因子。

The spectraplakin Short stop is an essential microtubule regulator involved in epithelial closure in .

作者信息

Takács Zsanett, Jankovics Ferenc, Vilmos Péter, Lénárt Péter, Röper Katja, Erdélyi Miklós

机构信息

Institute of Genetics, Biological Research Centre of the Hungarian Academy of Sciences, Temesvári krt. 62, Szeged 6726, Hungary.

Institute of Genetics, Biological Research Centre of the Hungarian Academy of Sciences, Temesvári krt. 62, Szeged 6726, Hungary

出版信息

J Cell Sci. 2017 Feb 15;130(4):712-724. doi: 10.1242/jcs.193003. Epub 2017 Jan 6.

DOI:10.1242/jcs.193003
PMID:28062848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5339884/
Abstract

Dorsal closure of the embryonic epithelium provides an excellent model system for the analysis of molecular mechanisms regulating cytoskeletal rearrangements. In this study, we investigated the function of the spectraplakin Short stop (Shot), a conserved cytoskeletal structural protein, during closure of the dorsal embryonic epithelium. We show that Shot is essential for the efficient final zippering of the opposing epithelial margins. By using isoform-specific mutant alleles and genetic rescue experiments with truncated Shot variants, we demonstrate that Shot functions as an actin-microtubule cross-linker in mediating zippering. At the leading edge of epithelial cells, Shot regulates protrusion dynamics by promoting filopodia formation. Fluorescence recovery after photobleaching (FRAP) analysis and imaging of microtubule growth revealed that Shot stabilizes dynamic microtubules. The actin- and microtubule-binding activities of Shot are simultaneously required in the same molecule, indicating that Shot is engaged as a physical crosslinker in this process. We propose that Shot-mediated interactions between microtubules and actin filaments facilitate filopodia formation, which promotes zippering by initiating contact between opposing epithelial cells.

摘要

胚胎上皮的背侧闭合为分析调节细胞骨架重排的分子机制提供了一个极佳的模型系统。在本研究中，我们调查了保守的细胞骨架结构蛋白——光谱斑蛋白短停蛋白（Shot）在胚胎上皮背侧闭合过程中的功能。我们发现Shot对于相对上皮边缘的高效最终拉链化至关重要。通过使用异构体特异性突变等位基因以及用截短的Shot变体进行基因拯救实验，我们证明Shot在介导拉链化过程中作为肌动蛋白 - 微管交联剂发挥作用。在上皮细胞的前沿，Shot通过促进丝状伪足形成来调节突起动态。光漂白后荧光恢复（FRAP）分析和微管生长成像显示Shot稳定动态微管。Shot的肌动蛋白结合和微管结合活性在同一分子中同时需要，这表明Shot在该过程中作为物理交联剂起作用。我们提出，Shot介导的微管与肌动蛋白丝之间的相互作用促进丝状伪足形成，而丝状伪足形成通过启动相对上皮细胞之间的接触来促进拉链化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/718aee4c7773/joces-130-193003-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/d2490495ab1b/joces-130-193003-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/dd9d5f414e22/joces-130-193003-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/5accc747fa9b/joces-130-193003-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/9a367be6b1c2/joces-130-193003-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/4f290345f152/joces-130-193003-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/de3e39cef961/joces-130-193003-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/dbbfe06e16a2/joces-130-193003-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/718aee4c7773/joces-130-193003-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/d2490495ab1b/joces-130-193003-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/dd9d5f414e22/joces-130-193003-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/5accc747fa9b/joces-130-193003-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/9a367be6b1c2/joces-130-193003-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/4f290345f152/joces-130-193003-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/de3e39cef961/joces-130-193003-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/dbbfe06e16a2/joces-130-193003-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f212/5339884/718aee4c7773/joces-130-193003-g8.jpg

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