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. 2020 Sep 25;11:4873. doi: 10.1038/s41467-020-18526-1

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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. 6 — Integration across genetic, transcriptomic, and epigenomic levels in ASD. ASD risk variants primarily act with respect to neuronal genes, which are broadly down-regulated, likely indirectly, including via micro-RNA (e.g. yellow module). Other features, including another microRNA module (brown), and DNA hypomethylation are predicted to be compensatory or secondary and are associated with up-regulation of glial-immune genes. Histone acetylation patterns show a complex relationship, with some predicted to reflect an attempt to compensate for changes in gene expression (e.g. M4), while others are predicted to be likely driving the changes (microglia). Blue bar-headed and red arrows correspond to regulatory mechanisms predicted to decrease and increase gene expression, respectively.