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Updated: Feb 9, 2026
Mouse Oocyte Microinjection, Maturation and Ploidy Assessment
Published on: July 23, 2011
SIRT4 is essential for metabolic control and meiotic structure during mouse oocyte maturation
Juan Zeng1, Manxi Jiang2, Xinghan Wu1
1State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
Abstract:
SIRT4 modulates energy homeostasis in multiple cell types and tissues. However, its role in meiotic oocytes remains unknown. Here, we report that mouse oocytes overexpressing SIRT4 are unable to completely progress through meiosis, showing the inadequate mitochondrial redistribution, lowered ATP content, elevated reactive oxygen species (ROS) level, with the severely disrupted spindle/chromosome organization. Moreover, we find that phosphorylation of Ser293-PDHE1α mediates the effects of SIRT4 overexpression on metabolic activity and meiotic events in oocytes by performing functional rescue experiments. By chance, we discover the SIRT4 upregulation in oocytes from aged mice; and importantly, the maternal age-associated deficient phenotypes in oocytes can be partly rescued through the knockdown of SIRT4. These findings reveal the critical role for SIRT4 in the control of energy metabolism and meiotic apparatus during oocyte maturation and indicate that SIRT4 is an essential factor determining oocyte quality.
Insights
SIRT4 overexpression impairs oocyte maturation by disrupting mitochondrial function and spindle organization. Reducing SIRT4 levels in aged oocytes partially rescues these age-associated defects, highlighting SIRT4
Area of Science:
- Cell Biology
- Reproductive Biology
- Metabolism
Background:
- SIRT4 is known to regulate energy homeostasis in various tissues.
- Its specific function in oocyte meiosis remains unexplored.
Purpose of the Study:
- To investigate the role of SIRT4 in mouse oocyte maturation.
- To determine the impact of SIRT4 on oocyte metabolism and meiotic progression.
Main Methods:
- Overexpression and knockdown of SIRT4 in mouse oocytes.
- Assessment of mitochondrial redistribution, ATP levels, reactive oxygen species (ROS), and spindle/chromosome organization.
- Functional rescue experiments involving phosphorylation of Ser293-PDHE1α.
- Analysis of SIRT4 expression in oocytes from aged mice.
Main Results:
- SIRT4 overexpression led to incomplete meiotic progression, poor mitochondrial distribution, reduced ATP, elevated ROS, and disrupted spindle/chromosome organization.
- Phosphorylation of Ser293-PDHE1α was identified as a mediator of SIRT4's effects on oocyte metabolism and meiosis.
- SIRT4 levels were upregulated in oocytes from aged mice.
- Knockdown of SIRT4 partially rescued age-associated oocyte defects.
Conclusions:
- SIRT4 plays a critical role in controlling energy metabolism and meiotic apparatus organization during oocyte maturation.
- SIRT4 is a key determinant of oocyte quality, particularly in the context of aging.
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