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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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Interactions within the expanded inherited axonopathy modules. (A,B) First degree interactions within CMT2 (A) and HSP (B) expanded modules. DIAMOnD proteins are separated into ribosomal proteins (green) and other (blue). Size of DIAMOnD nodes are proportional to DIAMOnD order of incorporation – smaller nodes were incorporated earlier. (C,D) First degree interaction counts between disease protein and ribosomal DIAMOnD proteins. (E) Relationships between HSP ribosomal DIAMOnD proteins, CMT ribosomal DIAMOnD proteins, and ribosomal proteins significantly localized to the axons of human motor neurons (q-value ≤ 0.1) (F). Distribution of log fold changes between axonal and soma differential localization.