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. 2019 Feb 8;9:1692. doi: 10.1038/s41598-018-37119-z

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© The Author(s) 2019

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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Inherited axonopathy proto-module connectivity (A–D) and expanded module networks (E,F). (A,B) Increased observed largest connected component (LCC) size of CMT2 (A) and HSP (B) disease seed genes in comparison to the expected, random distribution. (C,D) Increased shortest distance between inherited axonopathy disease genes in comparison to the expected, random expectation. (E,F) First degree interactions between known Mendelian disease genes (colored) and DIAMOnD genes (gray) for CMT2 (E) and HSP (F). Disease specific genes are labeled, and direct edges between disease genes are more heavily weighted.