Yingmei Wang, Hongjiang Li, Liji You, Shuhui Wang, Jinglei Bie, Ziyang Su, Lanying Shi, You-Qiang Su
{"title":"RSPO2与GDF9:BMP15异源二聚体协同促进小鼠颗粒细胞和卵母细胞发育","authors":"Yingmei Wang, Hongjiang Li, Liji You, Shuhui Wang, Jinglei Bie, Ziyang Su, Lanying Shi, You-Qiang Su","doi":"10.1002/advs.202501973","DOIUrl":null,"url":null,"abstract":"<p><p>The generation of mature oocytes, a cornerstone of reproduction, relies on the coordinated interactions between oocytes and surrounding follicular somatic cells. Central to this process is the bidirectional communication between the oocyte and granulosa cells, mediated by oocyte-secreted factors (OSFs), including GDF9 and BMP15. While GDF9 and BMP15 are well-established regulators of oocyte and follicle development, the role of additional OSFs and their coordination with GDF9 and BMP15 remains largely unclear. Here, RSPO2 is identified as a key OSF that coordinates with the GDF9:BMP15 heterodimer to regulate granulosa cell development and enhance oocyte competence. RSPO2, primarily expressed in oocytes, interacts with GDF9:BMP15 to preserve transcriptomic integrity in preantral granulosa cells. This coordination is gene-specific, exhibiting either synergistic or antagonistic effects depending on the target genes, and involves crosstalk between CTNNB1- and SMAD2-dependent pathways. Conditional knockout of Rspo2 in oocytes causes severe defects in granulosa cell and oocyte development, leading to subfertility and earlier reproductive lifespan termination. Transcriptomic analysis shows that RSPO2 loss disrupts key granulosa cell genes (e.g., Amh, Ccnd2, Inhbb, Kitl) and compromises oocyte mitochondrial function, reducing developmental competence. These findings establish RSPO2 as an essential factor in the oocyte-granulosa cell regulatory loop, crucial for ovarian function and fertility.</p>","PeriodicalId":117,"journal":{"name":"Advanced Science","volume":" ","pages":"e01973"},"PeriodicalIF":14.3000,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"RSPO2 Coordinates with GDF9:BMP15 Heterodimers to Promote Granulosa Cell and Oocyte Development in Mice.\",\"authors\":\"Yingmei Wang, Hongjiang Li, Liji You, Shuhui Wang, Jinglei Bie, Ziyang Su, Lanying Shi, You-Qiang Su\",\"doi\":\"10.1002/advs.202501973\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The generation of mature oocytes, a cornerstone of reproduction, relies on the coordinated interactions between oocytes and surrounding follicular somatic cells. Central to this process is the bidirectional communication between the oocyte and granulosa cells, mediated by oocyte-secreted factors (OSFs), including GDF9 and BMP15. While GDF9 and BMP15 are well-established regulators of oocyte and follicle development, the role of additional OSFs and their coordination with GDF9 and BMP15 remains largely unclear. Here, RSPO2 is identified as a key OSF that coordinates with the GDF9:BMP15 heterodimer to regulate granulosa cell development and enhance oocyte competence. RSPO2, primarily expressed in oocytes, interacts with GDF9:BMP15 to preserve transcriptomic integrity in preantral granulosa cells. This coordination is gene-specific, exhibiting either synergistic or antagonistic effects depending on the target genes, and involves crosstalk between CTNNB1- and SMAD2-dependent pathways. Conditional knockout of Rspo2 in oocytes causes severe defects in granulosa cell and oocyte development, leading to subfertility and earlier reproductive lifespan termination. Transcriptomic analysis shows that RSPO2 loss disrupts key granulosa cell genes (e.g., Amh, Ccnd2, Inhbb, Kitl) and compromises oocyte mitochondrial function, reducing developmental competence. These findings establish RSPO2 as an essential factor in the oocyte-granulosa cell regulatory loop, crucial for ovarian function and fertility.</p>\",\"PeriodicalId\":117,\"journal\":{\"name\":\"Advanced Science\",\"volume\":\" \",\"pages\":\"e01973\"},\"PeriodicalIF\":14.3000,\"publicationDate\":\"2025-06-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advanced Science\",\"FirstCategoryId\":\"88\",\"ListUrlMain\":\"https://doi.org/10.1002/advs.202501973\",\"RegionNum\":1,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advanced Science","FirstCategoryId":"88","ListUrlMain":"https://doi.org/10.1002/advs.202501973","RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
RSPO2 Coordinates with GDF9:BMP15 Heterodimers to Promote Granulosa Cell and Oocyte Development in Mice.
The generation of mature oocytes, a cornerstone of reproduction, relies on the coordinated interactions between oocytes and surrounding follicular somatic cells. Central to this process is the bidirectional communication between the oocyte and granulosa cells, mediated by oocyte-secreted factors (OSFs), including GDF9 and BMP15. While GDF9 and BMP15 are well-established regulators of oocyte and follicle development, the role of additional OSFs and their coordination with GDF9 and BMP15 remains largely unclear. Here, RSPO2 is identified as a key OSF that coordinates with the GDF9:BMP15 heterodimer to regulate granulosa cell development and enhance oocyte competence. RSPO2, primarily expressed in oocytes, interacts with GDF9:BMP15 to preserve transcriptomic integrity in preantral granulosa cells. This coordination is gene-specific, exhibiting either synergistic or antagonistic effects depending on the target genes, and involves crosstalk between CTNNB1- and SMAD2-dependent pathways. Conditional knockout of Rspo2 in oocytes causes severe defects in granulosa cell and oocyte development, leading to subfertility and earlier reproductive lifespan termination. Transcriptomic analysis shows that RSPO2 loss disrupts key granulosa cell genes (e.g., Amh, Ccnd2, Inhbb, Kitl) and compromises oocyte mitochondrial function, reducing developmental competence. These findings establish RSPO2 as an essential factor in the oocyte-granulosa cell regulatory loop, crucial for ovarian function and fertility.
期刊介绍:
Advanced Science is a prestigious open access journal that focuses on interdisciplinary research in materials science, physics, chemistry, medical and life sciences, and engineering. The journal aims to promote cutting-edge research by employing a rigorous and impartial review process. It is committed to presenting research articles with the highest quality production standards, ensuring maximum accessibility of top scientific findings. With its vibrant and innovative publication platform, Advanced Science seeks to revolutionize the dissemination and organization of scientific knowledge.