Aberrant Expression of Mitochondrial SAM Transporter SLC25A26 Impairs Oocyte Maturation and Early Development in Mice

被引:2
|
作者
Cheng, Gui-ping [1 ]
Guo, Shi-meng [1 ]
Yin, Ying [2 ]
Li, Yuan-yuan [1 ]
He, Ximiao [2 ]
Zhou, Li-quan [1 ]
机构
[1] Huazhong Univ Sci & Technol, Inst Reprod Hlth, Tongji Med Coll, Wuhan, Peoples R China
[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Basic Med, Wuhan, Hubei, Peoples R China
基金
国家重点研发计划; 中国国家自然科学基金;
关键词
S-ADENOSYLMETHIONINE TRANSPORTER; BACTERIAL EXPRESSION; MOUSE OOCYTES; IDENTIFICATION; RECONSTITUTION; FUNCTIONALITY; METHYLATION; DEFICIENCY; METABOLISM; STRESS;
D O I
10.1155/2022/1681623
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The immature germinal vesicle (GV) oocytes proceed through metaphase I (MI) division, extrude the first polar body, and become mature metaphase II (MII) oocytes for fertilization which is followed by preimplantation and postimplantation development until birth. Slc25a26 is the gene encoding S-adenosylmethionine carrier (SAMC), a member of the mitochondrial carrier family. Its major function is to catalyze the uptake of S-adenosylmethionine (SAM) from cytosol into mitochondria, which is the only known mitochondrial SAM transporter. In the present study, we demonstrated that excessive SLC25A26 accumulation in mouse oocytes mimicked naturally aged oocytes and resulted in lower oocyte quality with decreased maturation rate and increased reactive oxygen species (ROS) by impairing mitochondrial function. Increased level of Slc25a26 gene impacted gene expression in mouse oocytes such as mt-Cytb which regulates mitochondrial respiratory chain. Furthermore, increased level of Slc25a26 gene in fertilized oocytes slightly compromised blastocyst formation, and Slc25a26 knockout mice displayed embryonic lethality around 10.5 dpc. Taken together, our results showed that Slc25a26 gene plays a critical role in oocyte maturation and early mouse development.
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页数:20
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