Miro1 regulates mitochondrial homeostasis and meiotic resumption of mouse oocyte

Miro1, a mitochondrial Rho GTPase1, is a kind of mitochondrial outer membrane protein involved in the regulation of mitochondrial anterograde transport and its subcellular distribution. Mitochondria influence reproductive processes of mammals in some aspects. Mitochondria are important for oocyte ma...

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Veröffentlicht in:Journal of cellular physiology 2022-12, Vol.237 (12), p.4477-4486
Hauptverfasser: Xue, Yue, Meng, Tie‐Gang, Ouyang, Ying‐Chun, Liu, Sai‐Li, Guo, Jia‐Ni, Wang, Zhen‐Bo, Schatten, Heide, Song, Chun‐Ying, Guo, Xing‐Ping, Sun, Qing‐Yuan
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Sprache:eng
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Zusammenfassung:Miro1, a mitochondrial Rho GTPase1, is a kind of mitochondrial outer membrane protein involved in the regulation of mitochondrial anterograde transport and its subcellular distribution. Mitochondria influence reproductive processes of mammals in some aspects. Mitochondria are important for oocyte maturation, fertilization and embryonic development. The purpose of this study was to evaluate whether Miro1 regulates mouse oocyte maturation by altering mitochondrial homeostasis. We showed that Miro1 was expressed in mouse oocyte at different maturation stages. Miro1 mainly distributed in the cytoplasm and around the spindle during oocyte maturation. Small interference RNA‐mediated Miro1 depletion caused significantly abnormal distribution of mitochondria and endoplasmic reticulum as well as mitochondrial dysfunction, resulting in severely impaired germinal vesicle breakdown (GVBD) of mouse oocytes. For those oocytes which went through GVBD in the Miro1‐depleted group, part of them were inhibited in meiotic prophase I stage with abnormal chromosome arrangement and scattered spindle length. Our results suggest that Miro1 is essential for maintaining the maturation potential of mouse oocyte. Miro1, a mitochondrial Rho GTPase1, is a kind of mitochondrial outer membrane protein involved in the regulation of mitochondrial anterograde transport and its subcellular distribution. We showed that Miro1 was expressed in mouse oocyte at different maturation stages. Small interference RNA‐mediated Miro1 deletion caused significantly abnormal mitochondrial distribution as well as mitochondrial dysfunction, resulting in severely impaired germinal vesicle breakdown (GVBD) of mouse oocytes. For those oocytes which went through GVBD, partly of the oocytes in the Miro1‐depleted group were inhibited in meiotic prophase I with abnormal chromosome arrangement and scattered spindle length.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.30890