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 <i>Obox1</i> 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, <i>Obox1</i> 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 <i>Obox1</i>-deficienct ovaries, accompanied by dysregulated steroidogenesis-related gene expression. Transcriptomic profiling of <i>Obox1</i> 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 <i>Obox1</i> deficient mice, along with increased expression of <i>Gdf9, Bmp15, Foxl2</i>, and NOTCH signaling components. These findings suggest that <i>Obox1</i> is essential for maintaining hormonal balance and ovulatory function through regulating oocyte-granulosa cell interactions and steroid hormone synthesis.

Authors

Institutions

Publication Details

Journal
Fundamental Research
Published
2025-04-19
DOI
https://doi.org/10.1016/j.fmre.2025.04.008
Primary Topic
Reproductive System and Pregnancy
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Obox1 deficiency impairs fertility in female mice

Zhenzhen Hou, Lan Kang, Kang Chen, Yan Bi et al.
Fundamental Research
Reproductive System and Pregnancy
article

Obox1 deficiency impairs fertility in female mice

Zhenzhen Hou, Lan Kang, Kang Chen, Yan Bi, Fan Hengyu, Li Wu, Jiang Zhu, Shaorong Gao, Yinli Zhang, Jiacheng Shen, Xiaocui Xu, Rongrong Le, Heping Bai, Chenxiang Xi, Xiaochen Kou, Hong Wang, Yixuan Wang, Chong Li, Ran Zhang, Wen Ye, Shaohua Xu, Yanhong Zhao, Yiliang Xu
article en

Abstract

OBOX1 is a maternal factor involved in oogenesis and follicle development, yet its specific role remains unclear. Here, we demonstrated that <i>Obox1</i> 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, <i>Obox1</i> 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 <i>Obox1</i>-deficienct ovaries, accompanied by dysregulated steroidogenesis-related gene expression. Transcriptomic profiling of <i>Obox1</i> 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 <i>Obox1</i> deficient mice, along with increased expression of <i>Gdf9, Bmp15, Foxl2</i>, and NOTCH signaling components. These findings suggest that <i>Obox1</i> is essential for maintaining hormonal balance and ovulatory function through regulating oocyte-granulosa cell interactions and steroid hormone synthesis.

Fundamental ResearchVol. 5(4)
Tongji University (CN), Shanghai East Hospital (CN), Shanghai First Maternity and Infant Hospital (CN), Zhejiang University (CN)
National Natural Science Foundation of China, Fudan University, Tsinghua University, Tongji University, Key Technologies Research and Development Program, National Key Research and Development Program of China, Fundamental Research Funds for the Central Universities
Gender equality
Openalex Percentile: Top 91%
Reproductive System and Pregnancy
DOIOpen Access PDFOpenAlex
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.