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Maternal EHMT2 is essential for homologous chromosome segregation by regulating Cyclin B3 in mouse oocytes

ABSTRACT: During oocyte growth, various epigenetic modifications gradually establish, accompanying by large amounts of mRNAs and proteins accumulate. However, progress has been slow regarding the relationship between epigenetic modification and meiosis. Here, using Gdf9-Cre to achieve oocyte-specific ablation of Ehmt2 (Euchromatic Histone Lysine Methyltransferase 2) from primordial follicle stage, we found that female mutant mice were infertile and oocyte-specific knockout of Ehmt2 caused the failure of homologous chromosome separation independent of persistently activated SAC during the first meiosis. Further studies revealed that lacking maternal Ehmt2 affected the transcriptional level of Ccnb3, and microinjection of exogenous Ccnb3 mRNA could partly rescue the failure of homologous chromosomes segregation. Of particular importance was that EHMT2 could directly interact with CCNB3, despite truncated the SET domain. Therefore, our findings highlight the novel function of maternal EHMT2 on the metaphase I-to-anaphase I transition in mouse oocyte: directly interacting with CCNB3 apart from regulating the transcription of Ccnb3.

ORGANISM(S): Mus musculus

PROVIDER: GSE153611 | GEO | 2021/06/01

REPOSITORIES: GEO

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The landscape of H3K9me2 and CTCF in mice GV oocytes

Project description:During oocyte growth, various epigenetic modifications are gradually established, accompanied by accumulation of large amounts of mRNAs and proteins. However, little is known about the relationship between epigenetic modifications and meiotic progression. Here, by using Gdf9-Cre to achieve oocyte-specific ablation of Ehmt2 (Euchromatic-Histone-Lysine-Methyltransferase 2) from the primordial follicle stage, we found that female mutant mice were infertile. Oocyte-specific knockout of Ehmt2 caused failure of homologous chromosome separation independent of persistently activated SAC during the first meiosis. Further studies revealed that lacking maternal Ehmt2 affected the transcriptional level of Ccnb3, while microinjection of exogenous Ccnb3 mRNA could partly rescue the failure of homologous chromosome segregation. Of particular importance was that EHMT2 regulated ccnb3 transcriptions by regulating CTCF binding near ccnb3 gene body in genome in oocytes. In addition, the mRNA level of Ccnb3 significantly decreased in the follicles microinjected with Ctcf siRNA. Therefore, our findings highlight the novel function of maternal EHMT2 on the metaphase I-to-anaphase I transition in mouse oocytes: regulating the transcription of Ccnb3.

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