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. 2017 Aug 29;7:9791. doi: 10.1038/s41598-017-09952-1

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© The Author(s) 2017

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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Active FMNL2 and -3 polymerize an F-actin meshwork around the Golgi complex. (a,b) B16-F1 cells devoid of endogenous FMNL2/3 expression were transfected with either C-terminally tagged full length FMNL variants (a) or identical constructs except for harboring a point mutation known to disrupt FH2 dependent F-actin binding (b). Note prominent phalloidin-stainable F-actin meshwork around the Golgi apparatus in the region where the formin is located (a, red arrows). Respective F-actin binding mutants were still recruited to the Golgi, but failed to induce such an actin network (b). (c) Co-immunoprecipitation of endogenous actin with FH1-FH2 formin fragments with or without I→A mutations, as indicated, confirming that they abrogated F-actin binding. i = input, s = supernatant, IP = immunoprecipitation fraction.