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H2A.Z is essential for maternal H3K4me3 establishment and meiotic progression in mouse oocytes [RNA-Seq]

ABSTRACT: A unique landscape of histone modifications is established during mouse oogenesis. For example, H3K4me3 forms noncanonically broad domains (ncH3K4me3) at intergenic regions in transcriptionally quiescent fully grown oocytes (FGOs), which are briefly transmitted to early embryos. How such a unique landscape of histone modification is established during oogenesis remains to be elucidated. Here we examine the distributions of histone H2A variants and the roles of H2A.Z in ncH3K4me3 establishment in mouse oocytes. We show that H2A.Z is broadly distributed at distal regions, along with ncH3K4me3, in FGOs, whereas H2A, H2A.X, and TH2A are evenly distributed throughout the genome. Temporal profiling of H2A.Z distributions during oocyte growth reveals that noncanonically broad H2A.Z (ncH2A.Z) is established at the end of oocyte growth, concomitantly with ncH3K4me3 establishment. Depletion of H2A.Z by oocyte-specific conditional double knockout of H2A.Z.1 and H2A.Z.2 impairs ncH3K4me3 establishment and meiotic progression, resembling Mll2 KO oocytes. Moreover, depletion of ncH3K4me3 also causes loss of ncH2A.Z in Mll2 KO FGOs, indicating that ncH2A.Z and ncH3K4me3 are mutually dependent. Thus, our study reveals the critical role of H2A.Z in proper establishment of the maternal epigenome and oocyte development.

ORGANISM(S): Mus musculus

PROVIDER: GSE262049 | GEO | 2025/03/01

REPOSITORIES: GEO

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H2A.Z is essential for maternal H3K4me3 establishment and meiotic progression in mouse oocytes.

Project description:A unique landscape of histone modifications is established during mouse oogenesis. For example, H3K4me3 forms noncanonically broad domains (ncH3K4me3) at intergenic regions in transcriptionally quiescent fully grown oocytes (FGOs), which are briefly transmitted to early embryos. How such a unique landscape of histone modification is established during oogenesis remains to be elucidated. Here we examine the distributions of histone H2A variants and the roles of H2A.Z in ncH3K4me3 establishment in mouse oocytes. We show that H2A.Z is broadly distributed at distal regions, along with ncH3K4me3, in FGOs, whereas H2A, H2A.X, and TH2A are evenly distributed throughout the genome. Temporal profiling of H2A.Z distributions during oocyte growth reveals that noncanonically broad H2A.Z (ncH2A.Z) is established at the end of oocyte growth, concomitantly with ncH3K4me3 establishment. Depletion of H2A.Z by oocyte-specific conditional double knockout of H2A.Z.1 and H2A.Z.2 impairs ncH3K4me3 establishment and meiotic progression, resembling Mll2 KO oocytes. Moreover, depletion of ncH3K4me3 also causes loss of ncH2A.Z in Mll2 KO FGOs, indicating that ncH2A.Z and ncH3K4me3 are mutually dependent. Thus, our study reveals the critical role of H2A.Z in proper establishment of the maternal epigenome and oocyte development.

2025-03-01 | GSE262044 | GEO

Role of CxxC-finger Protein 1 in the Establishment of Epigenetic Landscapes in Mouse Oocytes

Project description:During oogenesis, oocytes gain competence to accomplish meiotic maturation and prepare for embryonic development following fertilization. Trimethylated histone H3 on lysine-4 (H3K4me3) mediates a wide range of nuclear events during these processes. Oocyte-specific knockout of CxxC-finger protein 1 (CXXC1, also known as CFP1), the chromatin-binding subunit of SETD1 methyltransferase, impairs the H3K4me3 accumulation during murine oogenesis and caused changes in chromatin configurations. This study investigated the changes of genomic H3K4me3 landscapes in oocytes after Cxxc1 knockout, as well as the influences of H3K4me3 changes on other epigenetic marks including DNA methylation, H3K27me3, H2AK119ub1, and H3K36me3. Chromatin immunoprecipitation and sequencing results indicated that H3K4me3 is globally decreased after abolishing Cxxc1, including both the promoter region and the gene body. The results also demonstrate that CXXC1 and another histone H3 methyltransferase MLL2 have nonoverlapping roles in mediating H3K4 trimethylation during oogenesis. In addition, Cxxc1 deletion caused a significant decrease of DNA methylation level in oocytes, and affected H3K27me3 and H2AK119ub1 distributions in the maternal genome, particularly at the regions that have high DNA methylation levels. The changes of epigenetic networks caused by Cxxc1 deletion correlated with transcription changes of the genes in the corresponding genomic regions. Taken together, this study provided mechanistic explanations underlying the phenotypes and molecular defects in Cxxc1 deleted oocytes, and highlighted a role of CXXC1 in orchestrating multiple factors to build up the appropriate epigenetic states of maternal genome during oocyte maturation.

2021-02-04 | GSE159581 | GEO

SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications (RRBS)

Project description:Splat-like 4 (Sall4) plays important roles in maintaining pluripotency of embryonic stem cells and in various developmental processes. Here, we find that the SALL4 null oocytes fail to undergo maturation to form fully-grown oocytes (FGOs) and subsequent meiosis resumption. We further discover that the loss of maternal SALL4 causes failure in establishment of DNA methylation. Moreover, we demonstrate that SALL4 modulates H3K4me3 and H3K27me3 modifications by regulating the expression of Kdm5b, Kdm6a and Kdm6b. Taken together, SALL4 plays pivotal roles in oocyte epigenetic maturation.

2017-03-07 | GSE84923 | GEO

SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications (RNA-Seq)

2017-03-07 | GSE84922 | GEO

Comparison of transcriptomes between Marf1+/+ (WT) and Marf1 ENU/ENU (Mutant) fully-grown oocytes (FGO)

Project description:Marf1 (MUT) female mice are infertile and the meiosis of the oocytes are arrest at prophase I. We thought to identify the potential causes of the meiotic arrest phenotype in the mutant oocytes by comparing the transcriptomes of the WT and mutant fully-grown oocytes (from 23-d old mice) that are transcriptional silent. We compared the transcriptomes of WT and MUT FGOs. 3 individual oocyte samples of each genotype (WT and MUT).

2012-03-30 | E-GEOD-31985 | biostudies-arrayexpress

MLL2 conveys transcription-independent H3K4me3 in the oocyte

Project description:Trimethylation of histone 3 lysine 4 (H3K4me3) is classically thought of as a mark of active promoters and yet it occurs at untranscribed domains. Partial redundancy of H3K4 methyltransferases has made it difficult to delineate the mechanisms underlying genomic targeting of H3K4me3. The oocyte provides an attractive system to investigate this, because extensive acquisition of H3K4me3 occurs in a non-dividing cell and ablation of a single H3K4 methyltransferase, Mll2, prevents most H3K4me3. We developed low-input chromatin immunoprecipitation to interrogate promoter associated histone modifications H3K4me3, H3K27ac and H3K27me3 throughout oogenesis. In non-growing oocytes, H3K4me3 was restricted to transcriptionally active promoters, but as oogenesis progresses, H3K4me3 accumulates in a transcription-independent manner: targeted to broad inter-genic regions, putative enhancers, and transcriptionally silent H3K27me3-marked promoters. Consequently, thousands of bivalent domains are established during oogenesis. Ablation of Mll2 resulted in loss of transcription-independent H3K4me3, with limited effects on transcription-coupled H3K4me3 or gene expression. Deletion of Dnmt3a/b showed that DNA methylation protects regions from acquiring H3K4me3. Our findings show that there are two independent mechanisms of targeting H3K4me3 to genomic elements, with MLL2 recruited to unmethylated CpG-rich regions independently of transcription.

2018-01-01 | GSE93941 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [RNA-seq]

Project description:Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at active gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) GV oocytes using ultra-low input ChIP-seq, in complement to DNA methylation and gene expression analysis. Setd1b cKO oocytes showed a redistribution of H3K4me3, with a marked loss at active gene promoters associated with downregulated gene expression. Remarkably, many regions gained H3K4me3 in Setd1b cKOs, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich. All of these are hallmarks of MLL2 targets; thus, loss of SETD1B appears to enable enhanced MLL2 activity. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to transcriptional activity and MLL2 to CpG content.

2022-01-17 | GSE167984 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [PBAT]

2022-01-17 | GSE167986 | GEO

Loss of SETD1B results in the redistribution of genomic H3K4me3 in the oocyte [ChIP-seq]

2022-01-17 | GSE167985 | GEO

Comparing the Transcriptomes of WT oocytes with Lsm14b KO oocytes by RNA-Seq Analysis

Project description:The success of human reproduction relies on high quality oocytes. Oocyte quality is manifested by the competence to complete meiosis, to be fertilized, and to support embryonic development. This meiotic and developmental competence is gradually established during the course of oocyte and follicle development, and is determined in large part by the autonomous gene expression program intrinsic to the oocyte. In order to explore the regulatory role of LSM14B in oocyte, we analyzed the effect of Lsm14b KO on gene expression in GV-stage fully-grown oocytes (FGOs) in mice by comparing the corresponding transcriptomes via RNA-Seq Analysis.

2023-09-08 | GSE204773 | GEO

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