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

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

PROVIDER: PRJNA643421 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12125000_1.fastq.gz	Fastqsanger.gz
	SRR12125000_2.fastq.gz	Fastqsanger.gz
	SRR12125001_1.fastq.gz	Fastqsanger.gz
	SRR12125001_2.fastq.gz	Fastqsanger.gz
	SRR12125002_1.fastq.gz	Fastqsanger.gz

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

Project description: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.

2021-06-01 | GSE153611 | GEO

Cyclin B3 is a dominant fast-acting cyclin that drives rapid early embryonic mitoses

Project description:Mitosis in early embryos often proceeds at a rapid pace, but how this pace is achieved is not understood. Here we show that cyclin B3 is the dominant driver of rapid embryonic mitoses in the C. elegans embryo. Cyclins B1 and B2 support slow mitosis (NEBD to Anaphase ~600s) but the presence of cyclin B3 dominantly drives the ~3-fold faster mitosis observed in wildtype. Multiple mitotic events are slowed down in Cyclin B1&B2-driven mitosis and cyclin B3-associated Cdk1 H1 kinase activity is ~25-fold more active than cyclin B1-associated Cdk1. Addition of cyclin B1 to fast cyclin B3-only mitosis introduces an ~60s delay between completion of chromosome alignment and anaphase onset; this delay, which is important for segregation fidelity, is dependent on inhibitory phosphorylation of the anaphase activator Cdc20. Thus, cyclin B3 dominance, coupled to a cyclin B1-dependent delay that acts via Cdc20 phosphorylation, sets the rapid pace and ensures mitotic fidelity in the early C. elegans embryo.

2024-07-29 | PXD053811 | Pride

Maternal EHMT2 is essential for homologous chromosome segregation by regulating <i>Cyclin B3</i> transcription in oocyte meiosis.

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.

| S-EPMC9295060 | biostudies-literature

Pelosinus fermentans B3 strain:B3

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The landscape of H3K9me2 and CTCF in mice GV oocytes

2024-08-22 | GSE182557 | GEO

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Project description:Halalkalicoccus jeotgali B3 genome sequencing

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DNA damage stress control is a tLT- and EHMT2-dependent central feature of Merkel Cell Carcinoma

Project description:Merkel cell carcinoma (MCC) is an aggressive skin cancer with a high mortality rate. Merkel cell polyomavirus (MCPyV) is the etiology of 80% of MCC cases via expression of the viral oncogenes small T antigen (sT) and truncated large T antigen (tLT). These proteins impair the Rb1-dependent G1/S checkpoint blockade and subvert the host cell epigenome to promote proliferation and evade immune detection. Through whole proteome analysis and proximal interactomics, we identified a tLT-dependent deregulation of DNA damage response (DDR) proteins. We investigated a novel protein proximal interaction between tLT and the histone methyltransferase EHMT2. In this regard, TA knockdown in MCC cells reduced DDR protein levels and increased levels of the DNA damage marker γH2Ax. EHMT2 normally promotes H3K9 methylation and DDR signaling. Given that inhibition of EHMT2 did not result in extensive proteomic changes, we hypothesized that the tLT-EHMT2 interaction could be involved in DDR pathway deregulation. In the presence of tLT, we report that EHMT2 gained double and single-strand break repair proximal interactors. EHMT2 inhibition rescued proliferation in MCC cells depleted for their T antigens, suggesting impaired DDR and/or lack of cell cycle checkpoint efficiency. Combined tLT and EHMT2 inhibition led to altered DDR signaling, evidenced by multiple alterations in signal transduction. Together, our data strongly suggest that tLT hijacks multiple components of the DNA damage machinery to enhance tolerance to DNA damage in MCC cells which could be at the basis of, the remarkable genetic stability of these cancers.

2024-06-04 | PXD044782 | Pride

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