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. 2019 Apr 15;9:6037. doi: 10.1038/s41598-019-42577-0

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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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CEP120 loss shows defective recruitment of the centriolar distal-end proteins C2CD3 and Talpid3. (a–c) KO-Con, KO-1, and KO-2 cells were synchronized at G2 phase and analyzed by immunofluorescence confocal microscopy using antibodies against Talpid3 (a), C2CD3 (b), CP110 (c), and SAS-6 (a–c), and the results were quantified. Histogram illustrating the relative intensity of Talpid3 (a), C2CD3 (b), and CP110 (c) on procentrioles. (d) The protein expression levels of endogenous CEP120, Talpid3 and C2CD3 were examined by immunoblotting using the indicated antibodies. Uncropped blots are shown in Fig. S6a. Error bars represent the mean ± s.d. ***P < 0.001; NS, not significant. Scale bar, 1 μm.