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. 2022 Apr 19;13(4):377. doi: 10.1038/s41419-022-04837-2

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© The Author(s) 2022

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 — A In normal conditions, UHRF1 in SCs controls a coordinated transcriptional program of ECM and cell adhesion genes (Timp1, Trf, and Spp1, et al.) in SCs by regulating its CG methylation, which usually plays a critical role in the coordinated homeostasis of adhesion between SC-GC and the cyclical disassembly versus reassembly of BTB. B In UHRF1-deficient SCs, the expressions of ECM and cell adhesion genes (Timp1, Trf, and Spp1) were upregulated due to their DNA demethylation, which leads to BTB disruption, junction defects, and inadequate cell adhesion, thereby resulting in a massive loss of immature germ cells from the seminiferous epithelium.