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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

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

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

2012-03-28 | GSE34864 | GEO

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]

2019-05-01 | GSE112834 | GEO

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

2019-05-01 | GSE112833 | GEO

Identification of maternal imprinting control regions (ICRs) in the post-implantation mouse embryo.

2012-10-04 | GSE32687 | GEO

Identification of maternal imprinting control regions (ICRs) in the post-implantation mouse embryo.

Project description:Genomewide DNA methylation profiles, generated by MeDIP-seq, for 8.5dpc wildtype and Dnmt3l-/+ mouse embryos were compared to identify differentially methylated regions (DMRs) that depend on the activity of the de novo DNA methyltransferase cofactor Dnmt3l in the oocyte. These DMRs were further characterised by their methylation state in mature mouse sperm and in the livers of inter-subspecies newborn mice. Maternal ICRs were identified by hypomethylation in Dnmt3l-/+ embryos as well as sperm, and maternal allele-specific methylation in liver. MeDIP-seq for two pools of wildtype and two pools of Dnmt3l-/+ mouse 8.5dpc embryos, the sperm of three sires, and 12 pools of three different embryonic livers each. Sliding window read count comparison between wildtype and Dnmt3l-/+ embryos, and between wildtype embryos and sperm samples. Read count comparison between the parental alleles at known SNP sites in inter-subspecies liver data.

2012-10-04 | E-GEOD-32687 | biostudies-arrayexpress

NLRP14 deficiency contributes to female infertility and early embryo arrest

Project description:Oocyte maturation is vital to attain full competence required fertilization and embryogenesis. As a maternal effect factor, NLRP14 is preferentially expressed in mammalian oocytes and early embryos. Yet the role and molecular mechanism of NLRP14 in oocyte maturation and early embryogenesis is largely unknown. Whether NLRP14 deficiency accounts for human infertility with oocyte and embryo defects remains to be elucidated. Here, NLRP14 is identified essential for establishment of competent oocytes that can sustain early embryo development. Maternal deficiency of Nlrp14 results in sterility characterized by oocyte maturation defects and early embryo arrest. Nlrp14 ablation leads to compromised oocyte quality and developmental competence due to impaired oocyte cytoplasmic and nuclear maturation. Mechanistically, NLRP14 interacts with UHRF1 in oocyte cytoplasm to protect it from proteasome-dependent degradation, and perturbs maternal mRNA zygotic-decay and zygotic genome activation during maternal-zygotic transition. Furthermore, compound heterozygous pathogenic variants in NLRP14 gene are identified in infertile women with early embryonic arrest, which interrupt the NLRP14-UHRF1 interaction or UHRF1 protein expression. Our data uncover a vital role of NLRP14 as a new cytoplasmic-specific modulator of UHRF1 in oocyte meiotic maturation and early embryogenesis, which should provide new insights into risk prediction and genetic diagnosis for female infertility.

2024-06-01 | GSE234001 | GEO

Genome-wide maps of DNA methylome during oocyte aging and its transgenerational inheritance

Project description:The goals of this study are to compare genome-wide DNA methylation levels in young and aged oocytes,and to investigate the transgenerational inheritance of methylome profiles in oocytes during natural aging. We apply a novel protocol of rapamycin to overcome the DNA methylation drift associated with oocyte aging. 8-week-old female mice were injected intraperitoneally with rapamycin or vehicle for 40 weeks. At the end of the experiment, females (48 weeks, F0) were paired with young adult (~4 mo old) males to produce F1 offspring (OF1 and ORaF1). An F2 generation (OF2 and ORaF2) resulted from mating F1 female at 44~48 weeks of age with young adult males. To generate YF1 and YF2 as normal control (offspring of young mother), we mated females (~8 weeks) with young adult males. Then we collect oocytes (F0,F1 and F2 generations)，sperm ( F1 and F2 generations) and hippocampus (F1 female offspring) from different groups to investigate the transgenerational inheritance of DNA methylome profiles associated with oocyte aging by the single cell whole-genome methylation sequencing (sc-WGBS). We found that oocytes from aged mother exhibited increased DNA methylation levels in CpG sites. Maternal aging related methylome changes can be inherited transgenerationally though oocyte to the germ line of F1 and F2 offspring. The application of rapamycin during the course of oocyte aging could reverse these DNA methylation alterations, and it can ameliorate several neurobehavioral aging trails that were in observed in aged oocyte offspring. WGBS-seq on DNA from hippocampal tissue revealed a number of differentially methylated (P<0.05) genes in OF1 and ORaF1 compared with YF1, and some of the enriched pathways were associated with aging process, such as PI3K-Akt signaling pathway (akin to transcriptional alterations above), MAPK signaling and Ras signaling pathway .

2022-12-31 | GSE164139 | GEO

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