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Publication : Methionine Adenosyltransferase 2β Participates in Mouse Oocyte Maturation by Regulating the MAPK Pathway.

First Author  An Q Year  2020
Journal  Reprod Sci Volume  27
Issue  1 Pages  163-171
PubMed ID  32046373 Mgi Jnum  J:310057
Mgi Id  MGI:6759272 Doi  10.1007/s43032-019-00015-6
Citation  An Q, et al. (2020) Methionine Adenosyltransferase 2beta Participates in Mouse Oocyte Maturation by Regulating the MAPK Pathway. Reprod Sci 27(1):163-171
abstractText  The methionine adenosyltransferase 2beta gene (Mat2b) encodes for the regulatory subunit of methionine adenosyltransferase (MAT), which catalyzes the biosynthesis of S-adenosylmethionine. MAT2B interacts with G protein-coupled receptor kinase interacting ArfGAP1 to increase the activity of extracellular signal-regulated kinases (ERKs) for the regulation of cell growth, metabolism, and differentiation. ERK activity is also essential for oocyte meiosis in mice. However, the regulatory role of MAT2B in mouse oocyte meiosis remains unclear. Accordingly, this study investigated the effect of MAT2B on mouse oocyte maturation. Immunostaining showed that MAT2B localized predominantly in the nucleus of fully grown germinal vesicle (GV) oocytes. After germinal vesicle breakdown (GVBD), MAT2B homogeneously localized in the cytoplasm. A low oocyte maturation rate was observed in Mat2b siRNA-treated oocytes. Furthermore, Mat2b knockdown repressed the phosphorylation of ERK1/2 and consequently blocked MAPK. Denuded oocytes treated with 20 muM U0126 mainly blocked MAPK phosphorylation and affected oocyte maturation. The oocytes arrested at GVBD and metaphase I (MI) by Mat2b silencing or U0126 treatment had several types of abnormal microtubule assembly. Furthermore, Mat2b knockdown or U0126 treatment resulted in the aberrant expression of six maternal transcripts, namely, Fgf8, Cdc2, Gdf9, Padi6, Polr2d, and Tecb2. To the best of our knowledge, this study is the first to demonstrate that Mat2bs play an important role in mouse oocyte maturation though MAPK signaling.
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