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. 2023 Jan 4;6:9. doi: 10.1038/s42003-022-04392-8

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© The Author(s) 2023

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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Fig. 2 — a WT, PFN1^+/− and PFN1^−/− RPE1 cells at anaphase stained for DNA (Hoechst 33342, blue), a midzone marker (Aurora B kinase, magenta) and Profilin 1 (green); scale bars 5 μm. Note that PFN1-KO cells show normal Aurora B localisation. b WT, PFN1^+/− and PFN1^−/− RPE1 cells at telophase stained for DNA (Hoechst 33342, blue), Profilin 1 (green) and F-actin (phalloidin, magenta). Arrowheads point towards furrow ingression; scale bars 5 μm. c Mean fluorescence intensity of phallodin staining at the cleavage furrow; data are shown as mean ± s.e.m.; dots represent the fluorescent intensity for each sample (n = 10 for WT, 11 for PFN1^+/−, 9 for PFN1^−/− cells); ***P = 0.0004, ****P < 0.0001, *P = 0.0461. Ordinary one-way ANOVA performed.