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. 2018 Jul 31;9:2992. doi: 10.1038/s41467-018-05385-0

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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. 7 — Model representing the differential requirement for Jag1 in the normal and transformed intestinal epithelial cells. As shown in the figure, MFNG in normal intestinal stem cells glycosylate Notch1 thus favoring its activation mediated by the Dll4 ligand that is localized in the adjacent (Paneth) cells. In contrast, non-glycosylated Notch1 present in the MFNG-negative tumor cells cannot respond to Dll4 leading to Jag1, which makes them addicted to Jag1-dependent Notch signaling