| First Author | Jiang Y | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 532 |
| Issue | 3 | Pages | 336-340 |
| PubMed ID | 32873390 | Mgi Jnum | J:304266 |
| Mgi Id | MGI:6694713 | Doi | 10.1016/j.bbrc.2020.08.055 |
| Citation | Jiang Y, et al. (2020) Loss of GM130 does not impair oocyte meiosis and embryo development in mice. Biochem Biophys Res Commun 532(3):336-340 |
| abstractText | 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. |
