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. 2020 Oct 12;13:43. doi: 10.1186/s13072-020-00364-6

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© The Author(s) 2020

Open AccessThis 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. 6 — Graphical summary showing the H3K27ac mediated activation of Hydra homologs of wnt5a, wnt11, brachyury, goosecoid and pitx. Wnt signaling causes enrichment of H3K27ac on the enhancer-like elements and it is associated with transcriptional activation. Upon inhibition of the histone demethylase JMJD3/UTX (KDM6A/B), the intergenic cis-regulatory regions cannot be demethylated and are therefore not accessible for deposition of the acetyl mark on the H3K27 residue. This leads to the downregulation of the Wnt target genes and thereby disrupts Wnt directed morphogenesis in Hydra