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. 2022 Nov 2;611(7936):532–539. doi: 10.1038/s41586-022-05377-7

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© The Author(s) 2022

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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Extended Data Fig. 10 — Overview of results from this pan-cortical characterization of the ASD transcriptome. Top left, differential gene expression signatures in ASD, while observed cortex-wide, show greatest effect size changes in posterior regions, especially BA17. Top right, a widespread posterior-predominant attenuation in transcriptomic regional identity is observed in ASD. Bottom, co-expression networks provide an organizing framework for interpretation of cortex-wide and regionally variable effects. A cortex-wide, upregulated co-expression module (isoM37) comprised of genes involved in proteostasis is enriched for common ASD-associated genetic variation. A cortex-wide, downregulated module characterized by genes involved in synaptic signaling and plasticity showed enrichment for common and rare genetic risk variants. Other modules exhibiting cortex-wide or regionally pronounced differential expression patterns in ASD are highlighted.