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. 2021 Apr 1;12:2021. doi: 10.1038/s41467-021-21917-7

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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. 4 — a Significance levels for the enrichment for genetic heritability in different DMRs (+/-25kb) and complex traits. Both conserved and human-specific neuronal DMRs are associated with schizophrenia. Enrichment with FDR < 0.05 are highlighted in squares. Notably, CG DMRs hypomethylated in NeuN+ cells compared to OLIG2+ cells in all three species (conserved NeuN+ hypo) are highly enriched in variants for several brain-related traits, and human-specific NeuN+ hypo shows enrichment in schizophrenia. b A sliding-window analysis further demonstrates that the aforementioned signal for schizophrenia was centered at the DMRs and did not originate from extended adjacent regions. The y-axis represents the P-values in sliding windows around DMRs classified by species (human or chimpanzee), cell-type (NeuN+ or OLIG2+), and cytosine context (mCG or mCH). Source data are provided as a Source Data file.