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Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE242960 | GEO | 2024/09/12

REPOSITORIES: GEO

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Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [CUT&TAG]

Project description:Zygotic gene activation (ZGA) is the first transcription event in life, and is associated with extensive epigenetic reprogramming, which is involved with dynamic incorporation of histone variant H3.3. H3.3 plays essential roles during mouse pre-implantation development. However, the coexistence of distinct sources of H3.3 in early embryos, including paternal and maternal allele-expressed H3.3 (paH3.3 and maH3.3), complicates our ability to track their individual dynamics, which may have distinct roles in embryonic development. In this study, by taking advantage of our H3.3B-HA-tagged mouse model, we illustrated the paH3.3 and maH3.3 landscapes in mouse early embryos, and described the manner of maternal mRNAs-derived H3.3 (mH3.3) on paternal genome reprogramming. We found the deposition of mH3.3 is required for cleavage development and minor ZGA, mechanistically, by mH3.3S31p-meditated acetylation at lysine 27. And, we propose that the mH3.3K27ac modification displaces the repressive histone modifications, thus enabling the activation of minor ZGA genes. Taken together, we demonstrate the central role of mH3.3 in reprogramming parental genomes by establishment of H3K27ac.

2024-09-12 | GSE242958 | GEO

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [ChIP-seq]

2024-09-12 | GSE242957 | GEO

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [RNA-seq]

2024-09-12 | GSE242959 | GEO

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation

Project description:Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation

| PRJNA1015611 | ENA

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [CUT&TAG]

Project description:Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [CUT&TAG]

| PRJNA1015619 | ENA

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [ChIP-seq]

Project description:Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [ChIP-seq]

| PRJNA1015620 | ENA

Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [RNA-seq]

Project description:Maternal H3.3-Mediated Reprogramming of Parental Genomes during Minor Zygotic Genome Activation [RNA-seq]

| PRJNA1015624 | ENA

Endodermal Maternal Transcription Factors Establish Super-Enhancers during Zygotic Genome Activation.

Project description:Elucidation of the sequence of events underlying the dynamic interaction between transcription factors and chromatin states is essential. Maternal transcription factors function at the top of the regulatory hierarchy to specify the primary germ layers at the onset of zygotic genome activation (ZGA). We focus on the formation of endoderm progenitor cells and examine the interactions between maternal transcription factors and chromatin state changes underlying the cell specification process. Endoderm-specific factors Otx1 and Vegt together with Foxh1 orchestrate endoderm formation by coordinated binding to select regulatory regions. These interactions occur before the deposition of enhancer histone marks around the regulatory regions, and these TFs recruit RNA polymerase II, regulate enhancer activity, and establish super-enhancers associated with important endodermal genes. Therefore, maternal transcription factors Otx1, Vegt, and Foxh1 combinatorially regulate the activity of super-enhancers, which in turn activate key lineage-specifying genes during ZGA.

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H3.3 kinetics predicts chromatin compaction status of parental genomes in early embryos.

Project description:BackgroundAfter fertilization, the fusion of gametes results in the formation of totipotent zygote. During sperm-egg fusion, maternal factors participate in parental chromatin remodeling. H3.3 is a histone H3 variant that plays essential roles in mouse embryogenesis.MethodsHere, we used transgenic early embryos expressing H3.3-eGFP or H2B-mCherry to elucidate changes of histone mobility.ResultsWe used FRAP analysis to identify that maternally stored H3.3 has a more significant change than H2B during maternal-to-embryonic transition. We also found that H3.3 mobile fraction, which may be regulated by de novo H3.3 incorporation, reflects chromatin compaction of parental genomes in GV oocytes and early embryos.ConclusionsOur results show that H3.3 kinetics in GV oocytes and early embryos is highly correlated with chromatin compaction status of parental genomes, indicating critical roles of H3.3 in higher-order chromatin organization.

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Symmetrically dimethylated histone H3R2 promotes global transcription during minor zygotic genome activation in mouse pronuclei.

Project description:Paternal genome reprogramming, such as protamine-histone exchange and global DNA demethylation, is crucial for the development of fertilised embryos. Previously, our study showed that one of histone arginine methylation, asymmetrically dimethylated histone H3R17 (H3R17me2a), is necessary for epigenetic reprogramming in the mouse paternal genome. However, roles of histone arginine methylation in reprogramming after fertilisation are still poorly understood. Here, we report that H3R2me2s promotes global transcription at the 1-cell stage, referred to as minor zygotic genome activation (ZGA). The inhibition of H3R2me2s by expressing a histone H3.3 mutant H3.3R2A prevented embryonic development from the 2-cell to 4-cell stages and significantly reduced global RNA synthesis and RNA polymerase II (Pol II) activity. Consistent with this result, the expression levels of MuERV-L as minor ZGA transcripts were decreased by forced expression of H3.3R2A. Furthermore, treatment with an inhibitor and co-injection of siRNA to PRMT5 and PRMT7 also resulted in the attenuation of transcriptional activities with reduction of H3R2me2s in the pronuclei of zygotes. Interestingly, impairment of H3K4 methylation by expression of H3.3K4M resulted in a decrease of H3R2me2s in male pronuclei. Our findings suggest that H3R2me2s together with H3K4 methylation is involved in global transcription during minor ZGA in mice.

| S-EPMC8115239 | biostudies-literature

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