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. 2023 Oct 13;14:6446. doi: 10.1038/s41467-023-41919-x

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© The Author(s) 2023

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. 8 — a Scheme illustrating the regulatory and topological changes in the GB genome including loss of long-range interactions, gain of promoter-promoter loops, redistribution of active chromatin marks towards SMAD3 and PITX1 sites and upregulation of genes related to synapse organization, axon guidance and axonogenesis. b Illustration depicting that SMAD3 inhibition and stimulation of neural activity cooperate to promote proliferation of GB cells in co-culture with glutamatergic neurons.