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. 2020 Oct 9;11:5114. doi: 10.1038/s41467-020-18643-x

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© The Author(s) 2020

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 — Wnt ligands from the matrix activate Wnt signaling in both matrix and DP cells. Wnt activity in the DP induces the expression of Rspo that act on matrix cells to augment Wnt signaling by suppressing the inhibitory action of Znrf3/Rnf43 on Fzd receptors. This positive feedback loop maintains anagen. Fgf signaling in the DP uncoils this positive loop by repressing Rspo and consequently induces catagen. Concomitantly to the reduction in Rspo expression, a negative feedback loop is activated by Wnt activity in the DP that upregulates the Wnt antagonists Dkk2 and Notum. The inhibitory action of these antagonists further dampens Wnt signaling in the matrix to synchronize catagen induction. Note that the absence and presence of multiple Wnt inhibitory pathways in the DP and matrix respectively allow Wnt activity in the DP to be uncoupled from Wnt activity in the matrix and thus enable the simultaneous incline and decline of Wnt activity in the DP and matrix, respectively. This illustration is created with BioRender.com.