ArticleScientific reports2016
Mitofusin-2 is required for mouse oocyte meiotic maturation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- Comparative developmental competence and gene expression in laparoscopically retrieved- and abattoir-derived goat oocytes.Frontiers in veterinary science · 2026Article
- Mitochondria-targeted antioxidant mitoquinone mitigates vitrification-induced damage in mouse ovarian tissue by maintaining mitochondrial homeostasis via the p38 MAPK pathway.European journal of medical research · 2024Article
- Nicotinamide Mononucleotide improves oocyte maturation of mice with type 1 diabetes.Nutrition & diabetes · 2024Article
- Mitofusins: from mitochondria to fertility.Cellular and molecular life sciences : CMLS · 2022Review
- All for one: changes in mitochondrial morphology and activity during syncytial oogenesis†.Biology of reproduction · 2022Article
- Uncovering the important role of mitochondrial dynamics in oogenesis: impact on fertility and metabolic disorder transmission.Biophysical reviews · 2021Review
- Potential of Mitochondrial Genome Editing for Human Fertility Health.Frontiers in genetics · 2021Review
- Mitofusin1 in oocyte is essential for female fertility.Redox biology · 2019Article
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitofusin-2 (Mfn2) is essential for embryonic development, anti-apoptotic events, protection against free radical-induced lesions, and mitochondrial fusion in many cells. However, little is known about its mechanism and function during oocyte maturation. In this study, we found that Mfn2 was expressed in the cytoplasm during different stages of mouse oocyte maturation. Mfn2 was mainly associated with α-tubulin during oocyte maturation. Knockdown of Mfn2 by specific siRNA injection into oocytes caused the mitochondrial morphology and quantity to change, resulting in severely defective spindles and misaligned chromosomes. This led to metaphase I arrest and the failure of first polar body extrusion. Furthermore, Mfn2 depletion from GV stage oocytes caused the redistribution of p38 MAPK in oocyte cytoplasm. These findings provide insights into potential mechanisms of Mfn2-mediated cellular alterations, which may have significant implications for oocyte maturation.
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