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RSPO2与GDF9:BMP15异二聚体协同作用以促进小鼠颗粒细胞和卵母细胞发育。

RSPO2 Coordinates with GDF9:BMP15 Heterodimers to Promote Granulosa Cell and Oocyte Development in Mice.

作者信息

Wang Yingmei, Li Hongjiang, You Liji, Wang Shuhui, Bie Jinglei, Su Ziyang, Shi Lanying, Su You-Qiang

机构信息

Shandong Provincial Key Laboratory of Animal Cell and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, 266237, China.

出版信息

Adv Sci (Weinh). 2025 Aug;12(30):e01973. doi: 10.1002/advs.202501973. Epub 2025 Jun 10.

Abstract

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.

摘要

成熟卵母细胞的生成是生殖的基石,它依赖于卵母细胞与周围卵泡体细胞之间的协同相互作用。这一过程的核心是卵母细胞与颗粒细胞之间的双向通讯,由卵母细胞分泌因子(OSF)介导,包括生长分化因子9(GDF9)和骨形态发生蛋白15(BMP15)。虽然GDF9和BMP15是卵母细胞和卵泡发育的公认调节因子,但其他OSF的作用及其与GDF9和BMP15的协调作用仍不清楚。在这里,R-spondin 2(RSPO2)被确定为一个关键的OSF,它与GDF9:BMP15异二聚体协同调节颗粒细胞发育并增强卵母细胞的能力。RSPO2主要在卵母细胞中表达,与GDF9:BMP15相互作用以维持窦前颗粒细胞的转录组完整性。这种协调是基因特异性的,根据靶基因表现出协同或拮抗作用,并且涉及β-连环蛋白1(CTNNB1)依赖性途径和SMAD2依赖性途径之间的串扰。卵母细胞中Rspo2的条件性敲除导致颗粒细胞和卵母细胞发育的严重缺陷,导致生育力下降和生殖寿命提前终止。转录组分析表明,RSPO2的缺失破坏了关键的颗粒细胞基因(如抗缪勒管激素(Amh)、细胞周期蛋白D2(Ccnd2)、抑制素βB(Inhbb)、干细胞因子(Kitl)),损害了卵母细胞的线粒体功能,降低了发育能力。这些发现确立了RSPO2作为卵母细胞-颗粒细胞调节回路中的一个重要因子,对卵巢功能和生育能力至关重要。

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