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. 2018 May 30;118(11):1410–1418. doi: 10.1038/s41416-018-0118-6

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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. 1 — LGR5 has a well-defined function in the promotion of Wnt/β-catenin signalling in normal intestinal stem cells. Without RSPO bound to LGR5, Wnt signalling is kept low through the action of transmembrane E3 ligases RNF43/ZNRF3, which internalise and degrade the Wnt receptors Frizzled and LRP5/6. This leads to downstream β-catenin degradation and subsequent repression of Wnt target genes. The binding of RSPO to LGR5 sustains Wnt signalling by neutralising the RNF43/ZNF3 ligases, which can no longer remove Wnt receptors from the cell membrane. FZD and LRP5/6 are free to bind Wnt ligands leading to stabilised β-catenin and downstream activation of Wnt target genes such as c-MYC, CyclinD1 and Axin2