Unique Broad Histone Lysine 4 Methylation Domains in Mouse Oocytes and Dynamic Regulation during Maternal to Zygotic Transition
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ABSTRACT:
PROVIDER: PRJNA295056 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2297300_1.fastq.gz | Fastqsanger.gz | |||
| SRR2297300_2.fastq.gz | Fastqsanger.gz | |||
| SRR2297310.fastq.gz | Fastqsanger.gz | |||
| SRR2297320_1.fastq.gz | Fastqsanger.gz | |||
| SRR2297320_2.fastq.gz | Fastqsanger.gz |
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Project description:The maternal to zygotic transition (MZT) involves the transfer of genome regulation from the oocyte to the embryo and is essential for the formation of totipotent embryos. However, regulatory mechanisms are still poorly understood despite recent progress in mapping the dynamics in RNA transcripts and DNA methylation1-9. Previous studies suggest that dynamic histone modifications may play important roles in MZT10-12, however direct measurements of chromatin states has been hindered by technical difficulties in profiling histone modifications from small quantities of cells. We have developed a micro-scale chromatin immunoprecipitation and sequencing (μChIP-seq) method and used it to profile histone H3 lysine methylation (H3K4me3) and acetylation (H3K27ac) genome-wide in the mouse oocyte, 2- cell and 8-cell stage embryo. Strikingly, we show that ~22% of the oocyte genome is associated with broad H3K4me3 domains that are anti-correlated with DNA methylation. Most H3K4me3 signal is rapidly lost and constricted to TSS regions in 2-cell embryos, concomitant with the onset of major zygotic genome activation (ZGA). We provide evidence that these broad H3K4me3 domains are established by Mll2 and actively removed by Kdm5a and Kdm5b, and likely play instrumental roles in MZT by defining regions of DNA demethylation in oocytes and the 2-cell embryo. Furthermore, broad H3K4me3 domains specify H3K27ac patterns in the early embryo and ZGA genes are generally related to broad H3K4me3 domains, suggesting a fundamental role in MZT. Our results provide insights into how the developmental program can be set up in the oocyte and transferred to the zygotic genome.
2016-09-08 | GSE72784 | GEO
Project description:The importance of germline-inherited posttranslational histone modification in priming early mammalian development is just emerging1-4. Histone H3 lysine 9 (H3K9) trimethylation is associated with heterochromatin and gene repression during cell-fate change5, while histone H3 lysine 4 (H3K4) trimethylation marks active gene promoters6. Mature oocytes are transcriptionally quiescent and possess remarkably broad domains of H3K4me3 (bdH3K4me3)1, 2. It remains unknown, which factors contribute to the maintenance of the bdH3K4me3 landscape. Lysine-specific demethylase 4A (KDM4A) demethylates H3K9me3 at promoters marked by H3K4me3 in actively transcribing somatic cells7. Here, we report that KDM4A-mediated H3K9me3 demethylation at bdH3K4me3 in oocytes is crucial for normal preimplantation development and zygotic genome activation (ZGA) after fertilization. Loss of KDM4A in oocytes causes extensive and aberrant H3K9me3 spreading at bdH3K4me3, resulting in insufficient transcriptional activation ZGA genes, endogenous retroviral elements and long terminal repeat -initiated chimeric transcripts in 2-cell embryos. The catalytic activity of KDM4A is essential for normal epigenetic reprogramming and preimplantation development. Hence, KDM4A plays a crucial role in preserving maternal epigenome integrity required for proper ZGA and transfer of developmental control to the embryo.
| EGAS00001004220 | EGA
Project description:Maternal-to-zygotic transition (MZT) is the first and key step in the control of animal development and is intimately related to changes of chromatin structure and histone modifications. Mono-ubiquitination of histone H2A at lysine-119 (H2AK119ub1), an important epigenetic modification in regulating chromatin configuration and function, is primarily catalyzed by polycomb repressive complex 1 (PRC1) and contributes to resistance to transcriptional reprogramming in mouse embryos. In this study, the genome-wide dynamic distribution of H2AK119ub1 during MZT in mice was investigated by chromosome immunoprecipitation and sequencing. The results indicated that H2AK119ub1 accumulated in fully grown oocytes, enriched at the transcriptional start sequences (TSSs) of maternal genes, but was promptly removed after meiotic resumption, particularly at the TSSs of early zygotic genes, by a previously unidentified mechanism. Genetic evidences indicated that ubiquitin-specific peptidase 16 (USP16) is the major deubiquitinase of H2AK119ub1 in mouse oocytes. Conditional knockout of Usp16 in oocytes did not impair their survival, growth, andor meiotic maturation. However, oocytes lacking USP16 were unable to undergo zygotic genome activation or gain developmental competence after fertilization, due to high levels of H2AK119ub1 deposition on the zygotic genomes. Taken together, this study indicates that H2AK119ub1 is erased during oocyte maturation by an USP16-dependent mechanism, which ensures zygotic genome reprogramming and transcriptional activation of essential early zygotic genes.
2022-06-05 | GSE154412 | GEO
Project description:Maternal-to-zygotic transition (MZT) is essential for the formation of a new individual, but is still poorly understood despite recent progress in analysis of gene expression and DNA methylation in early embryogenesis. Dynamic histone modifications may have important roles in MZT, but direct measurements of chromatin states have been hindered by technical difficulties in profiling histone modifications from small quantities of cells. Recent improvements allow for 500 cell-equivalents of chromatin per reaction, but require 10,000 cells for initial steps or require a highly specialized microfluidics device that is not readily available. We developed a micro-scale chromatin immunoprecipitation and sequencing (μChIP-seq) method, which we used to profile genome-wide histone H3 lysine methylation (H3K4me3) and acetylation (H3K27ac) in mouse immature and metaphase II oocytes and in 2-cell and 8-cell embryos. Notably, we show that ~22% of the oocyte genome is associated with broad H3K4me3 domains that are anti-correlated with DNA methylation. The H3K4me3 signal becomes confined to transcriptional-start-site regions in 2-cell embryos, concomitant with the onset of major zygotic genome activation. Active removal of broad H3K4me3 domains by the lysine demethylases KDM5A and KDM5B is required for normal zygotic genome activation and is essential for early embryo development. Our results provide insight into the onset of the developmental program in mouse embryos and demonstrate a role for broad H3K4me3 domains in MZT.
| S-EPMC6283663 | biostudies-literature
Project description:Sirtuin-1 (Sirt1), a NAD+-dependent histone deacetylase, exhibits several properties of a versatile driver of maternal-zygotic transition, due to its epigenetic and non-epigenetic substrates. The study was aimed at the dynamics of Sirt1 in early embryos and the contribution to maternal-zygotic transition. A conditional Sirt1-deficient knock-out mouse model was used. Females were hormonally stimulated and used as oocyte donors. oocytes were parthenogenetically activated and Sirt1-/- two-cell embryos were used for transcriptomic analysis.
2024-07-06 | E-MTAB-13483 | biostudies-arrayexpress
Project description:The importance of germline-inherited post-translational histone modifications on priming early mammalian development is just emerging1-4. Histone H3 lysine 9 (H3K9) trimethylation is associated with heterochromatin and gene repression during cell-fate change5, whereas histone H3 lysine 4 (H3K4) trimethylation marks active gene promoters6. Mature oocytes are transcriptionally quiescent and possess remarkably broad domains of H3K4me3 (bdH3K4me3)1,2. It is unknown which factors contribute to the maintenance of the bdH3K4me3 landscape. Lysine-specific demethylase 4A (KDM4A) demethylates H3K9me3 at promoters marked by H3K4me3 in actively transcribing somatic cells7. Here, we report that KDM4A-mediated H3K9me3 demethylation at bdH3K4me3 in oocytes is crucial for normal pre-implantation development and zygotic genome activation after fertilization. The loss of KDM4A in oocytes causes aberrant H3K9me3 spreading over bdH3K4me3, resulting in insufficient transcriptional activation of genes, endogenous retroviral elements and chimeric transcripts initiated from long terminal repeats during zygotic genome activation. The catalytic activity of KDM4A is essential for normal epigenetic reprogramming and pre-implantation development. Hence, KDM4A plays a crucial role in preserving the maternal epigenome integrity required for proper zygotic genome activation and transfer of developmental control to the embryo.
| S-EPMC7212036 | biostudies-literature
Project description:Conservation and species specificity are both unveiled in the reprogramming process of epigenetic modifications in early embryos. Pig is important agricultural livestock that closely related to human life and understanding the mechanisms of epigenetic reprogramming in porcine embryos could be assistive to the pig breeding industry and also informative to human embryo research. Nevertheless, current knowledge of epigenetic reprogramming in porcine embryos is elusive. We profile H3K4me3, H3K27me3, and H3K27ac modifications in porcine oocytes and preimplant embryos. Our data reveal the existence of unusual broad H3K4me3 domains not only in oocytes but also expanded in pre-ZGA embryos and demonstrates the extensive transitions of unusual broad H3K4me3 domains and their roles during embryogenesis. Notably, broad H3K27me3 and H3K27ac enriched domains are found to be preferably colocalized in these broad H3K4me3 domains when comparing to it in mice and human. By knocking down KDM5B in pig embryos, cleavage and developments were disrupted as demonstrated in mouse.
2022-07-08 | GSE163709 | GEO
Project description:Broad chromosomal domains of histone modification patterns in C. elegans
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Project description:Epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking
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Project description:Before zygotic genome activation (ZGA) the quiescent genome undergoes reprogramming to transition into the transcriptionally active state. However, the mechanisms underlying euchromatin establishment during early embryogenesis remain poorly understood. Here, we show that histone H4 lysine-16 acetylation (H4K16ac) is maintained from oocytes to fertilized embryos in Drosophila and mammals. H4K16ac forms large domains that control nucleosome accessibility of promoters prior to ZGA in flies. Maternal depletion of MOF acetyl-transferase leading to H4K16ac loss causes aberrant Pol II recruitment, compromises the 3D organization of the active genomic compartments during ZGA and consequently causes downregulation of post-zygotically expressed genes. Germline depletion of histone deacetylases revealed that other acetyl marks cannot compensate for H4K16ac loss in the oocyte. Moreover, zygotic re-expression of MOF was neither able to restore embryonic viability nor onset of X chromosome dosage compensation. Thus, maternal H4K16ac provides an instructive function to the offspring, priming future gene activation.
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