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. 2018 Aug 21;9:2862. doi: 10.1038/s41467-018-05099-3

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© The Author(s) 2018

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. 8 — Aberrant NG2 recycling is linked to differentiation defects. a Steady-state images of two single Lgl1 cKO cells monitored for NG2-EC (white dots) by TIRF, treated (bottom panel) or not treated (upper panel) with monensin. Pictures are acquired each 30 seconds. Note that NG2 is recycled to the membrane in non-treated cells (yellow arrow), whereas no recycling is observed in treated cells. Scale bar: 10 μm. b Fluorescent pictures illustrating Lgl1 cKO cells (Tom) monensin -treated or untreated and labeled for NG2 (blue) and O4 (red) after 5 days in differentiation conditions. Scale bar: 10 μm. c Graph representing quantification of O4+ and NG2+ cells in monensin-treated or untreated Lgl1 cKO cells. Untreated cells are mostly NG2+ and O4−, whereas treated cells show a reverse phenotype with a higher number of cells expressing O4. Data are depicted as mean ± s.e.m., n = 20 cells per genotype, three independent experiments (**p < 0.01, Student's t-test)