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. 2019 Sep 17;9:13462. doi: 10.1038/s41598-019-50058-7

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© The Author(s) 2019

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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A schematic diagram for the regulation of Sry expression by TET2 and JMJD1A. Epigenetic regulation of Sry expression through H3K9 demethylation and DNA demethylation in male gonad development. TET2 catalyzes DNA demethylation in the Sry promoter. It is conceivable that Sry expression levels in Tet2-deficient gonads might be higher than the threshold required for testis development. JMJD1A-mediated H3K9 demethylation plays a dominant role in Sry activation. Jmjd1a deficiency lead to substantial reduction of Sry expression, thereby inducing sex-reversal. We found that Tet2 deficiency synergistically enhanced the sex reversal phenotype of Jmjd1aΔ/Δ embryos.