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Sperm but not oocyte DNA methylome is inherited by zebrafish early embyros

ABSTRACT: 5-methylcytosine is a major epigenetic modification sometimes called "the fifth nucleotide". However, our knowledge of how offspring inherit the DNA methylome from parents is limited. We generated nine single-base resolution DNA methylomes including zebrafish gametes and early embryos. The oocyte methylome is significantly hypo-methylated compared to sperm. Strikingly, the paternal DNA methylation pattern is maintained throughout early embryogenesis. The maternal DNA methylation pattern is maintained until the 16-cell stage. Then, the oocyte methylome is gradually discarded through cell division, and progressively reprogrammed to a pattern similar to that of the sperm methylome. The passive demethylation rate and the de novo methylation rate are similar in the maternal DNA. By the midblastula stage, the embryo?s methylome is virtually identical to the sperm methylome. Moreover, inheritance of the sperm methylome facilitates the epigenetic regulation of embryogenesis. Therefore, besides DNA sequences, sperm DNA methylome is also inherited in zebrafish early embryos.

ORGANISM(S): Danio rerio

PROVIDER: GSE44075 | GEO | 2013/05/20

SECONDARY ACCESSION(S): PRJNA188516

REPOSITORIES: GEO

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Sperm but not oocyte DNA methylome is inherited by zebrafish early embyros

Project description:5-methylcytosine is a major epigenetic modification sometimes called "the fifth nucleotide". However, our knowledge of how offspring inherit the DNA methylome from parents is limited. We generated nine single-base resolution DNA methylomes including zebrafish gametes and early embryos. The oocyte methylome is significantly hypo-methylated compared to sperm. Strikingly, the paternal DNA methylation pattern is maintained throughout early embryogenesis. The maternal DNA methylation pattern is maintained until the 16-cell stage. Then, the oocyte methylome is gradually discarded through cell division, and progressively reprogrammed to a pattern similar to that of the sperm methylome. The passive demethylation rate and the de novo methylation rate are similar in the maternal DNA. By the midblastula stage, the embryo?s methylome is virtually identical to the sperm methylome. Moreover, inheritance of the sperm methylome facilitates the epigenetic regulation of embryogenesis. Therefore, besides DNA sequences, sperm DNA methylome is also inherited in zebrafish early embryos. hMeDIP-seq is performed in sperm,2-cell,16-cell,1k-cell and a input control sample 4 new samples are added to GSE44075. RNA-seq is performed in sperm, egg,1k-cell, germring samples .hMeDIP-seq is performed in sperm,2-cell,16-cell,1k-cell and a input control sample 10 new samples are added to GSE44075. Bisulfite-seq is performed for nine samples : sperm, egg,16-cell,32-cell,64-cell,128-cell,1k-cell , Germring and testis. TAB-seq is performed for one sample , 32-cell.

2013-05-20 | E-GEOD-44075 | biostudies-arrayexpress

Developmental enhancers revealed by extensive DNA methylome maps of zebrafish early embryos (MRE-seq)

Project description:DNA methylation undergoes dynamic changes during development and cell differentiation. Recent genome-wide studies discovered that tissue-specific differentially methylated regions (DMRs) often overlap tissue-specific distal cis-regulatory elements. However, developmental DNA methylation dynamics of the majority of the genomic CpGs outside gene promoters and CpG islands has not been extensively characterized. Here we generate and compare comprehensive DNA methylome maps of zebrafish developing embryos. From these maps, we identify thousands of developmental stage-specific DMRs (dsDMRs) across zebrafish developmental stages. The dsDMRs contain evolutionarily conserved sequences, are associated with developmental genes and are marked with active enhancer histone posttranslational modifications. Their methylation pattern correlates much stronger than promoter methylation with expression of putative target genes. When tested in vivo using a transgenic zebrafish assay, 20 out of 20 selected candidate dsDMRs exhibit functional enhancer activities. Our data suggest that developmental enhancers are a major target of DNA methylation changes during embryogenesis. MRE profiles of sperm and 2.5-hpf, 3.5-hpf, 4.5-hpf, 6-hpf and 24-hpf embryos were generated using Illumina HiSeq sequencing.

2015-02-13 | E-GEOD-52704 | biostudies-arrayexpress

Developmental enhancers revealed by extensive DNA methylome maps of zebrafish early embryos (MeDIP-seq)

Project description:DNA methylation undergoes dynamic changes during development and cell differentiation. Recent genome-wide studies discovered that tissue-specific differentially methylated regions (DMRs) often overlap tissue-specific distal cis-regulatory elements. However, developmental DNA methylation dynamics of the majority of the genomic CpGs outside gene promoters and CpG islands has not been extensively characterized. Here we generate and compare comprehensive DNA methylome maps of zebrafish developing embryos. From these maps, we identify thousands of developmental stage-specific DMRs (dsDMRs) across zebrafish developmental stages. The dsDMRs contain evolutionarily conserved sequences, are associated with developmental genes and are marked with active enhancer histone posttranslational modifications. Their methylation pattern correlates much stronger than promoter methylation with expression of putative target genes. When tested in vivo using a transgenic zebrafish assay, 20 out of 20 selected candidate dsDMRs exhibit functional enhancer activities. Our data suggest that developmental enhancers are a major target of DNA methylation changes during embryogenesis. MeDIP profiles of sperm and 2.5-hpf, 3.5-hpf, 4.5-hpf, 6-hpf and 24-hpf embryos were generated using Illumina HiSeq sequencing.

2015-02-13 | E-GEOD-52703 | biostudies-arrayexpress

A unique regulatory phase of DNA methylation in the early mammalian embryo

Project description:DNA methylation is highly dynamic during mammalian embryogenesis. It is broadly accepted that the paternal genome is actively depleted of global cytosine methylation at fertilization, followed by passive depletion that reaches a minimum at the blastocyst stage. However, this model is based on limited data, and to date no base-resolution maps exist to support and refine it. Here, we generated genome-scale DNA methylation maps in mouse gametes and through post-implantation embryogenesis. We find that the oocyte already exhibits global hypomethylation, most prominently at specific subfamilies of LINE-1 and LTR-containing retro-elements, which are disparate between gametes and resolve to lower methylation values in zygote. Surprisingly, the oocyte contributes a unique set of Differentially Methylated Regions (DMRs), including many CpG Island promoter regions, that are maintained in the early embryo but are lost at the onset of embryonic specification and absent in somatic cells. In contrast, sperm contributed methylation includes retrotransposons that become completely methylated after the blastocyst stage. Our data provide a complete genome-scale, base-resolution timeline of DNA methylation in the pre-specified embryo, when this epigenetic modification is most dynamic and before returning to the canonical somatic pattern. Comparison of DNA methylation patterns in mouse gametes and through embryogenesis using Reduced Representation Bisulfite Sequencing (RRBS)

2012-03-28 | E-GEOD-34864 | biostudies-arrayexpress

Danio rerio

Project description:Sperm but not oocyte DNA methylome is inherited by zebrafish early embyros

| PRJNA188516 | ENA

Methylome inheritance and enhancer dememorization construct an epigenetic gate safeguarding embryonic programs

Project description:Unlike that of mammals, the total DNA methylome of many cold-blooded vertebrates is globally inherited from gametes to early embryos. In zebrafish, this is however accompanied by sweeping “dememorization” of enhancers prior to fertilization for sperm and just after fertilization for oocyte, as they undergo full methylation and are not demethylated again until phylotypic stage. The significance of both global methylome inheritance and enhancer dememorization in early embryos remains largely unknown. Adding to the puzzles, the zygotic mutant zebrafish of dnmt1, the major DNA methylation maintenance methyltransferase, surprisingly can develop to term. To solve the role of DNA methylation in early development, we generated zebrafish embryos derived from dnmt1-knocking down oocytes using a recently developed method OMIS (Oocyte Microinjection in situ), which successfully eliminated DNA methylation before zygotic genome activation. dnmt1-deficient embryos failed to initiate epiboly and died around gastrulation. This is in part caused by activation of immune response and p53-regulated apoptosis, likely triggered by the derepression of transposable elements. Single cell RNA-seq further revealed defective differentiation in these mutants. DNA methylation is also required for the establishment of repressive histone marks H3K27me3 and H2AK119ub. Strikingly, the loss of DNA methylation leads to extensive derepression of somatic genes and enhancers, which acquire ectopic H3K27ac, accessible chromatin, and H3K4me3. These somatic enhancers are preferentially CG-rich and are bound by CG-containing TFs. By contrast, embryonic enhancers are generally CG-poor, methylation-insensitive, and are bound by CG-less TFs. Hence, the global DNA methylome inheritance is essential for vertebrate early development, and enhancer dememorization resets an epigenetic gate that separates embryonic and somatic programs.

2021-12-29 | GSE175951 | GEO

High-throughput sequencing of mRNA from oocyte, 1 cell, 16/32 cells, 128/256 cells, 3.5hpf and 5.3hpf zebrafish embryos (Wild type; AB line)

Project description:mRNA seq based approach to determine the transcriptome dynamics during early development To study the mechanisms regulating this developmental event in zebrafish, we applied RNA deep sequencing technology and generated comprehensive transcriptome profiles of 6 developmental stages from oocyte to early gastrulation. We determined the expression levels of maternal and zygotic transcripts and clustered them based on expression pattern. We identified a large number of novel transcribed regions in un-annotated regions of the genome, as well as splice variants with an estimated frequency of 40-75% during early zebrafish embryogenesis. Our data constitute a useful resource for developmental studies, gene discovery, and genome annotation. RNA was extracted from pooled embryos of desired stages and one RNA seq library was generated for each sample. Totally 6 stages were selected: Maternal, 1cell, 16/32 cells, 128/256 cells, 3.5hpf and 5.3hpf

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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [RNA-seq]

Project description:The oocyte epigenome plays critical roles in mammalian gametogenesis and embryogenesis. Yet, how it is established remains elusive. Here, we report that histone-lysine N-methyltransferase SETD2, an H3K36me3 methyltransferase, is a crucial regulator of the mouse oocyte epigenome. Deficiency in Setd2 leads to extensive alterations of the oocyte epigenome, including the loss of H3K36me3, failure in establishing the correct DNA methylome, invasion of H3K4me3 and H3K27me3 into former H3K36me3 territories and aberrant acquisition of H3K4me3 at imprinting control regions instead of DNA methylation. Importantly, maternal depletion of SETD2 results in oocyte maturation defects and subsequent one-cell arrest after fertilization. The preimplantation arrest is mainly due to a maternal cytosolic defect, since it can be largely rescued by normal oocyte cytosol. However, chromatin defects, including aberrant imprinting, persist in these embryos, leading to embryonic lethality after implantation. Thus, these data identify SETD2 as a crucial player in establishing the maternal epigenome that in turn controls embryonic development.

2019-05-01 | GSE112832 | GEO

SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [ChIP-seq]

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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [Bisulfite-seq]

2019-05-01 | GSE112833 | GEO