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. 2021 Mar 26;4:417. doi: 10.1038/s42003-021-01941-5

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© The Author(s) 2021

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. 7 — CENP-A overexpression reprograms cell fate with distinct effects on cell state and cell identity that depend on p53 status. Perturbation (a) by CENP-A overexpression (in blue) induces mitotic defects in both wild-type p53 (p53-WT, top panel blue) and p53-defective cells (p53-DN, dominant negative, bottom panel green). These defects provoke distinct cell fate decisions according to p53 status, impacting cell state (b) or identity (c). When p53 is functional, cell state shifts toward acute cell cycle arrest and senescence, reducing self-renewal capacity. Additional stress, like DNA damage from X-irradiation, amplifies this response, resulting in radiosensitivity. Furthermore, functional p53 ensures the preservation of epithelial identity. In contrast, when p53 is defective, the cells evade arrest and continue cycling, allowing CENP-A overexpression to promote epithelial–mesenchymal transition (EMT). * symbol: reprogramming stimulated by CENP-A overexpression.