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. 2018 Nov 19;9(12):1144. doi: 10.1038/s41419-018-1196-3

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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 — a The mRNA expression of Gdf9 and Bmp15 was decreased in oocytes of Rps26^fl/fl/Gdf9-Cre (RGC) mice compared to control (CTRL) Rps26^fl/fl mice. *p < 0.05 as calculated by two-tailed Student’s t-tests. b The mRNA expression of Cx37 was decreased in oocytes of Rps26^fl/fl/Gdf9-Cre (RGC) mice compared to control (CTRL) Rps26^fl/fl mice. *p < 0.05 as calculated by two-tailed Student’s t-tests. c Western blot results showing reduced expression of the Bmp15, Gdf9, and Cx37 proteins in PD12–14 ovaries from Rps26^fl/fl/Gdf9-Cre (RGC) mice compared with control (CTRL) Rps26^fl/fl mice. d The proposed working model. Generally, normal oocytes in primary follicles increase in mRNA synthesis activity mainly through RNA polymerase II, and they experience gradually increased levels of histone and DNA methylation, their nucleolus gradually transforms from the NSN to SN-type, and the follicles develop from pre-antral to antral follicles. Deletion of Rps26 in oocytes leads to reduced mRNA synthesis activity through downregulation of RNA polymerase II, and this leads to reduced levels of methylation modifications of histones and DNA and subsequent failure to transition from the NSN to SN-type. The oocytes secrete significantly lower levels of Gdf9, Bmp15, and Cx37, and this prevents follicle development from pre-antral follicles to antral follicles. In addition, inhibition of the PI3K/Akt/Foxo3a pathway in the ovary arrests the growth of NSN-type oocytes, and the oocytes finally die along with follicle degeneration, which ultimately leads to POF