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. 2019 Feb 4;9:1116. doi: 10.1038/s41598-018-38020-5

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Model of Cav1α function in the regulation of primary cilia length. In control cells (left), Cav1α localizes in non-caveolar domains at the apical membrane of MDCK cells, where it positively regulates RhoA activity. Active RhoA subsequently promotes apical actin polymerization through its effectors ROCK1 and DIA1. Actin meshwork rearrangement regulates ciliary lengthening by controlling the access of transport vesicles to the centrosomal zone. In the absence of Cav1α (right), RhoA activation is impaired and less apical actin polymerizes, allowing the arrival of more material at the centrosome that is used to assemble longer cilia.