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. 2019 Jul 5;10:2976. doi: 10.1038/s41467-019-10881-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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Fig. 5 — The ensheathment capacity of myelinating SCs is independent of mTOR signaling. mTOR deletion in Fbxw7 mutant nerves failed to suppress aberrant SC-axon interactions. Apparent multi-axonal myelination and SCs that appeared to both myelinate and encompass multiple small non-myelinated axons were present in both Dhh^cre(+);Fbxw7^fl/+;mTOR^+/+ (b, e) and Dhh^cre(+);Fbxw7^fl/+;mTOR^fl/fl (HetΔmTOR) (c, f) nerves. Neither phenotype was ever observed in sibling controls (a, d; p < 0.0001(****); ANOVA). Tracing the BL (e, f; white arrows) suggested these behaviors were the acts of single SCs. Both phenotypes were also present in the sole Dhh^cre(+);Fbxw7^fl/fl;mTOR^fl/fl (cKOΔmTOR) animal we were able to collect (g, h). Asterisks above bars indicate comparisons with controls; comparisons between Dhh^cre(+);Fbxw7^fl/+ and Dhh^cre(+);Fbxw7^fl/+;mTOR^fl/fl were not significant. P3: N = 4 control, 6 Dhh^cre(+);Fbxw7^fl//+;mTOR^+/+, 5 Dhh^cre(+);Fbxw7^fl/+;mTOR^fl/fl, 1 Dhh^cre(+);Fbxw7^fl/fl;mTOR^fl/fl. m = myelinated axon; a = unmyelinated axon. Error bars depict S.D.