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在小鼠卵细胞成熟过程中,波韦会扰乱G2/M转换并诱导介质停止

Yejin Kim¹, Yu-Jin Jo², Seung-Bin Yoon²

¹Primate Resources Center (PRC), Korea Research Institute of Bioscience and Biotechnology (KRIBB), Nengme-gil 351-33, Jeongeup-si, Jeollabuk-do 56216, Republic of Korea; Department of Biological Science, College of Natural Sciences, Wonkwang University, Iksan 54538, Republic of Korea.

Reproductive toxicology (Elmsford, N.Y.)

|August 21, 2025

概括

通过诱导DNA损伤和破坏关键信号通路,贝韦里辛 (BEA) 菌毒素会导致小鼠卵细胞的介质衰竭. 这种毒性作用阻断了卵细胞的成熟和生殖囊泡的分解.

科学领域:

生殖毒理学
分子生物学
菌类毒理学

背景情况:

波维 (BEA) 是一种已知具有生殖毒性的菌毒素.
对于BEA对卵细胞半球变异的影响的具体机制在很大程度上是未知的.
了解这些机制对于评估生殖风险至关重要.

研究的目的:

研究BEA在小鼠卵细胞中引起介质衰竭的分子机制.
阐明BEA对卵细胞成熟和相关信号通路的影响.

主要方法:

在实验室中暴露未成熟的小鼠卵细胞.
对DNA损伤,细胞循环调节和关键信号通路组件 (PI3K/AKT/PDE3A,cAMP,CDK/MPF) 的分析.
介质恢复和生殖囊泡分解 (GVBD) 的评估.

主要成果:

在卵细胞中引起显著的DNA损伤.
BEA 破坏了由酸丁3-激酶/蛋白激酶 B/基酶 3A (PI3K/AKT/PDE3A) 介导的 cAMP 信号通路.
通过Wee1和CDC25B改变CDK1活性,从而抑制成熟促进因子 (MPF) 的激活,导致胚芽囊停止.

结论:

在哺乳动物卵细胞中,BEA治疗阻断了生殖囊泡的分解和随后的介质性进展.
PI3K/AKT/PDE3A-cAMP-MPF通路的破坏是BEA诱导的卵细胞介质衰竭的关键机制.
由于影响卵细胞成熟,BEA对女性生殖健康构成重大风险.

关键词:

贝维里辛在CAMP-MPF路径中女性不孕症 G2/M 过渡时间转移性停止卵细胞成熟 PI3K/AKT信号提供生殖毒性

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