Loss of GM130 does not impair oocyte meiosis and embryo development in mice.

Yonghui Jiang, Yue Liu, Feng Han, Jingjing Zhou, Xinze Zhang, Junting Xu, Zhiheng Yu, Shigang Zhao, Fei Gao, Han Zhao

Biochemical and biophysical research communications 2020 Nov 12

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Golgi matrix protein 130 (GM130), encoded by GOLGA2, is the classical marker of the Golgi apparatus. It plays important roles in various mitotic events, such as interacting with importin-alpha and liberating spindle assembly factor TPX2 to regulate mitotic spindle formation. A previous study showed that in vitro knockdown of GM130 could regulate the meiotic spindle pole assembly. In the current study, we found that knockout (KO) mice progressively died, had a small body size and were completely infertile. Furthermore, we constructed an oocyte-specific GM130 knockout mouse model (GM130-ooKO) driven by Gdf9-Cre. Through breeding assays, we found that the GM130-ooKO mice showed similar fecundity as control mice. During superovulation assays, the KO and GM130-ooKO mice had comparable numbers of ovulated eggs, oocyte maturation rates and normal polar bodies, similar to the control groups. Thus, this study indicated that deletion of GM130 might have a limited impact on the maturation and morphology of oocytes. This might due to more than one golgin sharing the same function, with others compensating for the loss of GM130. Copyright © 2020 Elsevier Inc. All rights reserved.

Citation

Yonghui Jiang, Yue Liu, Feng Han, Jingjing Zhou, Xinze Zhang, Junting Xu, Zhiheng Yu, Shigang Zhao, Fei Gao, Han Zhao. Loss of GM130 does not impair oocyte meiosis and embryo development in mice. Biochemical and biophysical research communications. 2020 Nov 12;532(3):336-340