Obox1 deficiency impairs fertility in female mice
OBOX1 is a maternal factor involved in oogenesis and follicle development, yet its specific role remains unclear. Here, we demonstrated that Obox1 knockout female mice exhibit subfertility, characterized by reduced litter size and impaired ovulation. These oocytes show minimal disruption in early em...
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KeAi Communications Co. Ltd.
2025-07-01
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2667325825002055 |
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| author | Li Wu Jiacheng Shen Zhenzhen Hou Yinli Zhang Yan Bi Ran Zhang Heping Bai Wen Ye Kang Chen Jiang Zhu Chenxiang Xi Yiliang Xu Xiaochen Kou Yanhong Zhao Chong Li Hengyu Fan Rongrong Le Yixuan Wang Xiaocui Xu Shaohua Xu Hong Wang Shaorong Gao Lan Kang |
| author_facet | Li Wu Jiacheng Shen Zhenzhen Hou Yinli Zhang Yan Bi Ran Zhang Heping Bai Wen Ye Kang Chen Jiang Zhu Chenxiang Xi Yiliang Xu Xiaochen Kou Yanhong Zhao Chong Li Hengyu Fan Rongrong Le Yixuan Wang Xiaocui Xu Shaohua Xu Hong Wang Shaorong Gao Lan Kang |
| author_sort | Li Wu |
| collection | DOAJ |
| description | OBOX1 is a maternal factor involved in oogenesis and follicle development, yet its specific role remains unclear. Here, we demonstrated that Obox1 knockout female mice exhibit subfertility, characterized by reduced litter size and impaired ovulation. These oocytes show minimal disruption in early embryonic development post-fertilization. However, Obox1 deficiency leads to decreased levels of gonadotropins and female sex hormones, especially the luteinizing hormone (LH). Exogenous human chorionic gonadotropin (hCG) administration during superovulation failed to rescue the ovulation defect. Post-ovulation, the ovulation-related genes and serum progesterone levels were significantly reduced in Obox1-deficienct ovaries, accompanied by dysregulated steroidogenesis-related gene expression. Transcriptomic profiling of Obox1 deficient metaphase II (MII) oocytes revealed downregulation of genes involved in mitochondrial energy metabolism and biosynthesis, and upregulation of genes associated with cell transport, transcription, RNA processing, translation. Further investigation revealed that follistatin gene expression was upregulated in both MII oocytes and ovaries of Obox1 deficient mice, along with increased expression of Gdf9, Bmp15, Foxl2, and NOTCH signaling components. These findings suggest that Obox1 is essential for maintaining hormonal balance and ovulatory function through regulating oocyte-granulosa cell interactions and steroid hormone synthesis. |
| format | Article |
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| institution | Matheson Library |
| issn | 2667-3258 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | KeAi Communications Co. Ltd. |
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| series | Fundamental Research |
| spelling | doaj-art-ddddcfba332743a98a6c0cd2ee8e89f92025-07-28T04:16:41ZengKeAi Communications Co. Ltd.Fundamental Research2667-32582025-07-015415701580Obox1 deficiency impairs fertility in female miceLi Wu0Jiacheng Shen1Zhenzhen Hou2Yinli Zhang3Yan Bi4Ran Zhang5Heping Bai6Wen Ye7Kang Chen8Jiang Zhu9Chenxiang Xi10Yiliang Xu11Xiaochen Kou12Yanhong Zhao13Chong Li14Hengyu Fan15Rongrong Le16Yixuan Wang17Xiaocui Xu18Shaohua Xu19Hong Wang20Shaorong Gao21Lan Kang22Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaLife Sciences Institute, Zhejiang University, Hangzhou 310058, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaLife Sciences Institute, Zhejiang University, Hangzhou 310058, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, ChinaFrontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, ChinaShanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 201204, China; Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China; Corresponding authors.Institute for Regenerative Medicine, State Key Laboratory of Cardiovascular Diseases, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai 200123, China; Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai 200092, China; Corresponding authors.OBOX1 is a maternal factor involved in oogenesis and follicle development, yet its specific role remains unclear. Here, we demonstrated that Obox1 knockout female mice exhibit subfertility, characterized by reduced litter size and impaired ovulation. These oocytes show minimal disruption in early embryonic development post-fertilization. However, Obox1 deficiency leads to decreased levels of gonadotropins and female sex hormones, especially the luteinizing hormone (LH). Exogenous human chorionic gonadotropin (hCG) administration during superovulation failed to rescue the ovulation defect. Post-ovulation, the ovulation-related genes and serum progesterone levels were significantly reduced in Obox1-deficienct ovaries, accompanied by dysregulated steroidogenesis-related gene expression. Transcriptomic profiling of Obox1 deficient metaphase II (MII) oocytes revealed downregulation of genes involved in mitochondrial energy metabolism and biosynthesis, and upregulation of genes associated with cell transport, transcription, RNA processing, translation. Further investigation revealed that follistatin gene expression was upregulated in both MII oocytes and ovaries of Obox1 deficient mice, along with increased expression of Gdf9, Bmp15, Foxl2, and NOTCH signaling components. These findings suggest that Obox1 is essential for maintaining hormonal balance and ovulatory function through regulating oocyte-granulosa cell interactions and steroid hormone synthesis.http://www.sciencedirect.com/science/article/pii/S2667325825002055SubfertilityHormone deficiencyAbnormal luteinizationAberrant steroidogenesisOocyte-granulosa cell interactions |
| spellingShingle | Li Wu Jiacheng Shen Zhenzhen Hou Yinli Zhang Yan Bi Ran Zhang Heping Bai Wen Ye Kang Chen Jiang Zhu Chenxiang Xi Yiliang Xu Xiaochen Kou Yanhong Zhao Chong Li Hengyu Fan Rongrong Le Yixuan Wang Xiaocui Xu Shaohua Xu Hong Wang Shaorong Gao Lan Kang Obox1 deficiency impairs fertility in female mice Fundamental Research Subfertility Hormone deficiency Abnormal luteinization Aberrant steroidogenesis Oocyte-granulosa cell interactions |
| title | Obox1 deficiency impairs fertility in female mice |
| title_full | Obox1 deficiency impairs fertility in female mice |
| title_fullStr | Obox1 deficiency impairs fertility in female mice |
| title_full_unstemmed | Obox1 deficiency impairs fertility in female mice |
| title_short | Obox1 deficiency impairs fertility in female mice |
| title_sort | obox1 deficiency impairs fertility in female mice |
| topic | Subfertility Hormone deficiency Abnormal luteinization Aberrant steroidogenesis Oocyte-granulosa cell interactions |
| url | http://www.sciencedirect.com/science/article/pii/S2667325825002055 |
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