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多囊蛋白-1对微管细胞骨架的调节有利于粘着斑周转，从而调节细胞粘附和迁移。

Regulation of the microtubular cytoskeleton by Polycystin-1 favors focal adhesions turnover to modulate cell adhesion and migration.

作者信息

Castelli Maddalena, De Pascalis Chiara, Distefano Gianfranco, Ducano Nadia, Oldani Amanda, Lanzetti Letizia, Boletta Alessandra

机构信息

Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy.

Current Address: International PhD Program, Institut Pasteur, Paris, France.

出版信息

BMC Cell Biol. 2015 May 7;16:15. doi: 10.1186/s12860-015-0059-3.

DOI:10.1186/s12860-015-0059-3
PMID:25947155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4437554/
Abstract

BACKGROUND

Polycystin-1 (PC-1) is a large plasma membrane receptor, encoded by the PKD1 gene, which is mutated in most cases of Autosomal Dominant Polycystic Kidney Disease (ADPKD). The disease is characterized by renal cysts. The precise function of PC-1 remains elusive, although several studies suggest that it can regulate the cellular shape in response to external stimuli. We and others reported that PC-1 regulates the actin cytoskeleton and cell migration.

RESULTS

Here we show that cells over-expressing PC-1 display enhanced adhesion rates to the substrate, while cells lacking PC-1 have a reduced capability to adhere. In search for the mechanism responsible for this new property of PC-1 we found that this receptor is able to regulate the stability of the microtubules, in addition to its capability to regulate the actin cytoskeleton. The two cytoskeletal components are acting in a coordinated fashion. Notably, we uncovered that PC-1 regulation of the microtubule cytoskeleton impacts on the turnover rates of focal adhesions in migrating cells and we link all these properties to the capability of PC-1 to regulate the activation state of Focal Adhesion Kinase (FAK).

CONCLUSIONS

In this study we show several new features of the PC-1 receptor in modulating microtubules and adhesion dynamics, which are essential for its capability to regulate migration.

摘要

背景

多囊蛋白-1（PC-1）是一种大型质膜受体，由PKD1基因编码，在大多数常染色体显性多囊肾病（ADPKD）病例中发生突变。该疾病的特征是肾囊肿。尽管多项研究表明PC-1可响应外部刺激调节细胞形状，但其确切功能仍不清楚。我们和其他人报道过PC-1调节肌动蛋白细胞骨架和细胞迁移。

结果

我们在此表明，过表达PC-1的细胞对底物的黏附率增强，而缺乏PC-1的细胞黏附能力降低。在寻找导致PC-1这一新特性的机制时，我们发现该受体除了能够调节肌动蛋白细胞骨架外，还能够调节微管的稳定性。这两种细胞骨架成分以协同方式发挥作用。值得注意的是，我们发现PC-1对微管细胞骨架的调节影响迁移细胞中黏着斑的周转率，并且我们将所有这些特性与PC-1调节黏着斑激酶（FAK）激活状态的能力联系起来。

结论

在本研究中，我们展示了PC-1受体在调节微管和黏附动力学方面的几个新特征，这些特征对于其调节迁移的能力至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/c0a44530bc3c/12860_2015_59_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/a4036f627304/12860_2015_59_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/9536aeae0ffa/12860_2015_59_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/91ca391db266/12860_2015_59_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/4d4ba11ed221/12860_2015_59_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/7aad0a763137/12860_2015_59_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/c0a44530bc3c/12860_2015_59_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/a4036f627304/12860_2015_59_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/9536aeae0ffa/12860_2015_59_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/91ca391db266/12860_2015_59_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/4d4ba11ed221/12860_2015_59_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/7aad0a763137/12860_2015_59_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85db/4437554/c0a44530bc3c/12860_2015_59_Fig6_HTML.jpg

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