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Updated: Oct 26, 2025
Meiotic Spindle Assessment in Mouse Oocytes by siRNA-mediated Silencing
Published on: October 11, 2015
Melatonin Protects Against Mdivi-1-Induced Abnormal Spindle Assembly and Mitochondrial Superoxide Production During
Seul-Gi Yang1,2, Seung-Yeon Joe1,2, Jin-Wook Bae1,2
1Department of Biotechnology, College of Engineering, Daegu University, Gyeongsan, South Korea.
Abstract:
Mitochondrial division inhibitor 1 (Mdivi-1) reportedly provides a close connection between oocyte maturation and mitochondrial function in pigs. N-acetyl-5-methoxy-tryptamine (melatonin) is known to be a representative antioxidant with the ability to rehabilitate meiotic maturation of porcine oocytes. However, the ability of melatonin to recover Mdivi-1-mediated disruption of spindle formation during meiotic maturation of porcine oocytes during in vitro maturation (IVM) has not been studied. Here, we first investigated changes in mitochondrial length, such as fragmentation and elongation form, in mature porcine oocytes during IVM. Mature oocytes require appropriate mitochondrial fission for porcine oocyte maturation. We identified a dose-dependent reduction in meiotic maturation in porcine oocytes following Mdivi-1 treatment (50, 75, and 100 μM). We also confirmed changes in mitochondrial fission protein levels [dynamin-related protein 1 phosphorylation at serine 616 (pDRP1-Ser616) and dynamin-related protein 1 (DRP1)], mitochondrial membrane potential, and ATP production in 75 μM Mdivi-1-treated oocytes. As expected, Mdivi-1 significantly reduced mitochondrial function and DRP1 protein levels and increased spindle abnormalities in porcine oocytes. In addition, we confirmed that melatonin restores abnormal spindle assembly and reduces meiotic maturation rates by Mdivi-1 during porcine oocyte maturation. Interestingly, the expression levels of genes that reduce DNA damage and improve tubulin formation were enhanced during porcine meiotic maturation. Taken together, these results suggest that melatonin has direct beneficial effects on meiotic maturation through tubulin formation factors during porcine oocyte maturation.
Insights
Mitochondrial division inhibitor 1 (Mdivi-1) impairs pig oocyte maturation, but melatonin can restore spindle formation and improve maturation rates by enhancing tubulin factors.
Area of Science:
- Reproductive Biology
- Cell Biology
- Mitochondrial Dynamics
Background:
- Mitochondrial division inhibitor 1 (Mdivi-1) impacts porcine oocyte maturation and mitochondrial function.
- Melatonin, an antioxidant, can rehabilitate meiotic maturation in porcine oocytes.
Purpose of the Study:
- Investigate melatonin's ability to counteract Mdivi-1-induced disruption of spindle formation during porcine oocyte IVM.
- Examine changes in mitochondrial morphology, function, and protein levels during Mdivi-1 treatment.
- Assess melatonin's protective effects on spindle assembly and meiotic maturation.
Main Methods:
- Porcine oocytes were matured *in vitro* (IVM) with varying Mdivi-1 concentrations (50, 75, 100 μM).
- Mitochondrial length, membrane potential, ATP production, and DRP1 protein levels were analyzed.
- Spindle formation and meiotic maturation rates were assessed in Mdivi-1-treated and melatonin-rescued oocytes.
- Gene expression related to DNA damage and tubulin formation was evaluated.
Main Results:
- Mdivi-1 dose-dependently reduced meiotic maturation and mitochondrial function in porcine oocytes.
- Mdivi-1 treatment altered mitochondrial fission protein levels (pDRP1-Ser616, DRP1), reduced membrane potential, and decreased ATP production.
- Mdivi-1 increased spindle abnormalities and decreased maturation rates, effects reversed by melatonin.
- Melatonin enhanced expression of genes involved in DNA repair and tubulin formation.
Conclusions:
- Mdivi-1 disrupts porcine oocyte maturation by impairing mitochondrial function and spindle formation.
- Melatonin effectively restores normal spindle assembly and improves meiotic maturation rates in Mdivi-1-treated oocytes.
- Melatonin exerts beneficial effects via tubulin formation factors, suggesting a role in oocyte quality improvement.
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