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. 2019 Jan 24;9:597. doi: 10.1038/s41598-018-37160-y

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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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Mice lacking full-length Myo10 have intact brain commissures. (A) Schematic diagram illustrating the interaction of the cargo protein DCC (deleted in colorectal cancer) with the cargo-binding FERM domain of Myo10. (B) Colocalization of DCC and Myo10 to the tips of filopodia. HEK293T cells were transfected with human DCC and EGFP-tagged human Myo10 (hMyo10-EGFP), and subsequently fixed and labeled with anti-DCC antibodies which recognize an extracellular domain. Scale bar: 10 µm. (C) Coronal and horizontal sections of isolated and fixed mouse brains obtained by MRI (magnetic resonance imaging). Scale bars: 1 mm. CC, corpus callosum; AC, anterior commissure; HC, hippocampal commissure. (D) Schematic summary diagram. Mice lacking DCC (encoded by Dcc) or the DCC ligand Netrin-1 (encoded by Ntn1) have absent or negligible commissures, whereas commissures are intact in mice lacking the DCC transport protein Myo10.