在小鼠卵细胞半转化进展期间,KAT8在氧化还原稳定和线粒体动力学中的功能
Xuan Wu1, Shiwei Wang1, Yajun Guo1
1State Key Laboratory of Animal Biotech Breeding, National Engineering Laboratory for Animal Breeding, Key Laboratory of Animal Genetics, Breeding and Reproduction of the Ministry of Agriculture, College of Animal Science and Technology, China Agricultural University, Beijing, China.
概括
高水平的氨酸转移酶8 (KAT8) 通过抑制SOD1来破坏小鼠卵细胞成熟,导致线粒体功能障碍和缺陷. 这会影响卵细胞质量,特别是在晚年母亲的年龄.
科学领域:
- 生殖生物学 生殖生物学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 氨酸转化酶8 (KAT8) 参与各种生物过程.
- 对于KAT8在小鼠卵细胞成熟中的作用尚不清楚.
研究的目的:
- 为了研究KAT8对小鼠卵细胞成熟的影响.
- 阐明KAT8介导卵细胞缺陷背后的分子机制.
主要方法:
- 在小鼠卵细胞中过度表达Kat8 (Kat8-OE).
- 针对线粒体分布,ROS,γH2AX和α-tubulin的免疫染.
- 免疫沉以评估KAT8-SOD1相互作用.
- 对于SOD1表达的西方涂抹.
- 注射Myc-Sod1cRNA以评估救援效果.
主要成果:
- 过度表达Kat8导致成熟失败,减少GVBD和第一极体排放率.
- Kat8-OE卵细胞表现出异常的线粒体分布,增加ROS,γH2AX积累,并破坏了线圈组织.
- 过度表达KAT8降低了SOD1蛋白水平,并与SOD1.1相互作用.
- 证实SOD1下调是卵细胞质量下降的关键因素,部分由Myc-Sod1cRNA注射挽救.
结论:
- 升高的KAT8抑制SOD1活动,导致线粒体动力学缺陷,氧化还原失衡以及小鼠卵细胞成熟期间的螺旋/染色体失调.
- 这种机制有助于卵细胞质量下降,与晚年母亲的年龄相关.
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