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Published on: October 11, 2015
Aberrant Expression of Mitochondrial SAM Transporter SLC25A26 Impairs Oocyte Maturation and Early Development in Mice
Gui-Ping Cheng1, Shi-Meng Guo1, Ying Yin2
1Institute of Reproductive Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
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.
Insights
Excessive S-adenosylmethionine carrier (SLC25A26) in oocytes impairs mitochondrial function, reducing quality and maturation. Slc25a26 deficiency causes embryonic lethality, highlighting its critical role in development.
Area of Science:
- Reproductive biology
- Mitochondrial biology
- Developmental biology
Background:
- Oocyte maturation is crucial for female fertility and successful embryonic development.
- S-adenosylmethionine carrier (SLC25A26) transports S-adenosylmethionine into mitochondria, impacting cellular metabolism.
- Mitochondrial dysfunction is implicated in oocyte aging and reduced fertility.
Purpose of the Study:
- To investigate the role of Slc25a26 in mouse oocyte maturation and early embryonic development.
- To determine the effects of excessive SLC25A26 accumulation on oocyte quality and mitochondrial function.
- To assess the consequences of Slc25a26 deficiency on embryonic development.
Main Methods:
- Oocyte collection and maturation assays in mice.
- Assessment of oocyte quality, including maturation rate and reactive oxygen species (ROS) levels.
- Mitochondrial function analysis and gene expression profiling (e.g., mt-Cytb).
- Generation and analysis of Slc25a26 knockout mice for embryonic lethality studies.
Main Results:
- Excessive SLC25A26 accumulation in oocytes mimicked aged oocytes, decreasing maturation rates and increasing ROS by impairing mitochondrial function.
- Increased Slc25a26 levels affected gene expression, including mt-Cytb, involved in mitochondrial respiration.
- Elevated Slc25a26 compromised blastocyst formation, and Slc25a26 knockout mice exhibited embryonic lethality around 10.5 days post-coitum (dpc).
Conclusions:
- Slc25a26 plays a critical role in maintaining oocyte quality and mitochondrial function during maturation.
- Proper regulation of Slc25a26 is essential for successful early mouse development.
- Mitochondrial SAM transport is vital for reproductive success and embryonic viability.
