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. 2021 May 4;12:2508. doi: 10.1038/s41467-021-22815-8

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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 — AHL15 overexpression induces strong chromatin decondensation, coinciding with the induction of embryonic competence in somatic cells. This prevents chromosome segregation in some cells, leading to endomitosis events that give rise to polyploid embryonic cells and subsequently to polyploid somatic embryos. By contrast, 2,4-D treatment leads to enhanced AHL15 expression that is sufficient to induce somatic-to-embryonic reprogramming, but insufficient to induce the level of chromatin decondensation needed for endomitosis. However, when 2,4-D treatment is combined with a treatment that induces strong chromatin decondensation (TSA or heat stress), endomitosis does occur, giving rise to polyploid somatic embryos.