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. 2017 Apr 4;8:18. doi: 10.1186/s13229-017-0131-2

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 3 — Genetic variance in SDQ-ADHD and SCDC scores due to variation within K-RAS signalling upregulated genes. The genetic variance composition for SCDC and SDQ-ADHD scores in ALSPAC was dissected according to genetic variation within molecular signatures database (MSigDB) hallmark gene set collections [53]. For each measure, the genetic variance is shown for the pathway of K-RAS signalling upregulated genes including one standard error (grey bar) and measurement-specific p values (*p ≤ 0.05, **p ≤ 0.01 and ***p ≤ 0.001). Statistical evidence across measures was combined using a homogeneity statistic [55], accounting for phenotypic overlap among traits. The meta-analysis p value (meta-p) reflects four SCDC scores (at 8, 11, 14 and 17 years) and five SDQ-ADHD scores (7, 10 12, 13 and 17 years) and is Bonferroni-adjusted for 50 analysed pathways (pathway-adjusted). ALSPAC Avon Longitudinal Study of Parents and Children, SCDC Social and Communication Disorders Checklist at 8, 11, 14 and 17 years (rank-transformed), SDQ-ADHD ADHD subscale of the Strength and Difficulties Questionnaire at 7, 10 12, 13 and 17 years (rank-transformed)