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. 2024 Mar 22;25:77. doi: 10.1186/s13059-024-03212-y

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Loss of B-type lamins induces cell cycle arrest and altered nuclear morphology. A Propidium iodine staining in HCT116 and HCT116.^{LMN(B1&B2)−AID} cells to assess the percentages of cells in G1, S, and G2/M phase. Data are representative of three independent biological replicates (N = 3). B Flow cytometric analysis to measure relative DAPI-stained nuclear area from data collected with the ImageStreamX after 8 h of auxin treatment. Black: auxin-treated cells containing high mClover intensity. Green: auxin-treated cells with low or no mClover intensity. At least 20,000 events were recorded during the experiment. C Immunofluorescence shows the presence of nuclear blebbing in B-type lamin-deficient cells. Scale bar = 5 μm. Data are representative of three independent biological replicates (N = 3)