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. 2020 Nov 9;40(2):436–451. doi: 10.1038/s41388-020-01524-4

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© The Author(s) 2020

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. 4 — a Rescue of abnormal microtubule growth rates upon partial CDK1 inhibition in TP53/TP73-deficient cells. HCT116 and TP53/TP73-deficient cells were treated with the CDK1 inhibitor RO-3306 or with low-dose Taxol for 16 h and mitotic microtubule plus end assembly rates were measured. Scatter dot plots show average microtubule polymerization rates (20 microtubules/cell, n = 30 mitotic cells from three independent experiments, mean ± SD, t-test). b Rescue of abnormal microtubule growth rates upon partial CDK1 inhibition in CDKN1A-deficient cells. DLD-1 and DLD-1-CDKN1A^−/− cells were treated as in a and mitotic microtubule polymerization rates were determined (20 microtubules/cell, n = 30 mitotic cells from three independent experiments, mean ± SD, t-test). c Suppression of lagging chromosomes upon partial CDK1 inhibition in TP53/TP73-deficient cells. HCT116 and TP53/TP73-deficient cells were treated with the CDK1 inhibitor RO-3306 or with low-dose Taxol. The graph shows the proportion of cells exhibiting lagging chromosomes during anaphase (n = 300 anaphase cells from three independent experiments, mean ± SD, t-test). d Suppression of lagging chromosomes upon partial CDK1 inhibition in CDKN1A-deficient cells. Parental and CDKN1A-deficient DLD-1 cells were treated as in c. The graph shows the proportion of cells exhibiting lagging chromosomes during anaphase (n = 300 anaphase cells from three independent experiments, mean ± SD, t-test). e, f Mitotic microtubule growth rates in single-cell clones derived from control, TP53/TP73-deficient HCT116 cells or from parental and CDKN1A-deficient DLD-1 cells and treated with or without CDK1 inhibitor (RO-3306). Scatter dot plots show average microtubule growth rates (20 microtubules/cell, n = 10 mitotic cells for each clone, mean ± SD, t-test). g, h Chromosome number variability in single-cell clones derived from control, TP53/TP73-deficient HCT116 cells or from parental and CDKN1A-deficient DLD-1 cells and treated with or without CDK1 inhibitor. The proportion of cells with a chromosome number deviating from modal (45 chromosomes for HCT116, 46 chromosomes for DLD-1) was calculated for three independent clones (n = 50 cells per condition).