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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE242959 | GEO | 2024/09/12

REPOSITORIES: GEO

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

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 | GSE242957 | GEO

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

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Histone variant H3.3 is an essential maternal factor for oocyte reprogramming

Project description:Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming both for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA into oocytes in somatic cell nuclear transfer (SCNT) embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity. Transcriptome sequencing of 4-cell NT embryos, Luciferase 4-cell SCNT embryos, 4-cell NT embryos_H3.3KD, 4-cell NT embryos_H3.3KD+H3.3mRNA, H3.3 KD + H3.2 mRNA SCNT embryos

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Detection of newly synthesized RNA reveals transcriptional reprogramming during ZGA and a role of Obox3 in totipotency acquisition

Project description:Zygotic genome activation (ZGA) after fertilization is a conserved transcriptional activation process that enables the maternal-to-zygotic transition. However, the global view of ZGA, particularly at the initiation, is not yet completely understood. Here, we develop a method to capture and sequence newly synthesized RNA in the early mouse embryos, which provides a view of transcriptional reprogramming events during ZGA. Our data demonstrate that gene activation associated with major ZGA, previously thought to occur exclusively during the mid-to-late 2-cell stage, is already initiated in zygotes. Furthermore, we identify a set of genes activated during minor ZGA and observe an enrichment of the homeobox-containing Obox factor motif at the promoters of minor ZGA genes. Among several Obox factors, Obox3 overexpression in mouse embryonic stem cells activates ZGA genes. Notably, the expression of Obox3 is severely impaired in somatic cell nuclear transfer (SCNT) embryos, and restoring its expression corrects the ZGA profile and greatly improves SCNT embryo development. Hence, our study reveals the dynamic transcriptional reprogramming during ZGA and underscores the crucial role of Obox3 in facilitating totipotency acquisition.

2024-04-02 | GSE235547 | GEO

Histone variant H3.3 is an essential maternal factor for oocyte reprogramming

2014-06-02 | GSE56762 | GEO

Loss of DUX causes minor defects in zygotic genome activation and is compatible with mouse development

Project description:How maternal factors in oocytes trigger zygotic genome activation (ZGA) is a long-standing question in developmental biology. Recent studies in 2-cell like embryonic stem cells (2C-like cells) implicate that the DUX family transcription factors are key regulators of ZGA in placental mammals. To characterize the role of DUX in ZGA, we generated Dux cluster knockout (KO) mouse lines. Unexpectedly, we found both Dux zygotic KO (Z-KO) and maternal/zygotic KO (MZ-KO) embryos can survive to adulthood despite showing reduced developmental potential. Furthermore, transcriptome profiling of the MZ-KO embryos revealed that loss of DUX has minimal effect on ZGA and most DUX targets in 2C-like cells are normally activated in MZ-KO embryos. Thus, contrary to the key function in inducing 2C-like cells, our data indicate that DUX only has a minor role in ZGA and loss of DUX is compatible with mouse development.

2019-04-10 | GSE121746 | GEO

Quantitative proteomics reveals the dynamic proteome landscape of zebrafish embryos during maternal-to-zygotic transition and its relationship to zygotic genome activation

Project description:Upon fertilization, the embryonic genome remains transcriptionally inactive until the mid-blastula transition. Zygotic genome activation (ZGA) of vertebrate embryos has been extensively studied using nucleic acid-based strategies, but proteomics data are still scarce, impeding the full mechanistic understanding of how ZGA is executed during the maternal-to-zygotic transition (MZT). Here, we performed quantitative proteomics to decipher the proteome landscape of zebrafish embryos during the MZT, quantifying nearly 5,000 proteins across four embryonic stages. The stage-specific clustering based on protein expression pattern revealed that helicases (i.e., eif4a2 and ruvbl1) facilitate pluripotency factors (i.e., nanog, pou5f3, ctcf, and hmga1) triggering ZGA in zebrafish, accompanied by the maternal product decay with P-bodies and ubiquitin dependent proteolytic pathway. Dozens of transcription factors show wave-like expression patterns during MZT, implying their diverse functions in triggering the ZGA and modulating differentiation for organ development. The combination of morpholino knockdown and quantitative proteomics demonstrated that maternal Nanog is required for proper embryogenesis by regulating 1) interactions with other pluripotency factors, 2) F-actin band formation, 3) cell cycle checkpoints and 4) maternal product degradation. This study represents the most systematic proteomics survey of developmentally regulated proteins and their expression profiles accompanying MZT in zebrafish, which is a valuable proteome resource for understanding ZGA.

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Analysis of genome architecture during SCNT reveals a role of cohesin in impeding minor ZGA

Project description:Somatic cell nuclear transfer (SCNT) can reprogram a somatic nucleus to a totipotent state. However, the re-organization of three-dimensional chromatin structure in this process remains poorly understood. Using low-input Hi-C, we revealed that during SCNT, the transferred nucleus first enters a mitotic-like state (premature chromatin condensation). Unlike fertilized embryos, SCNT embryos show stronger TADs at the 1-cell stage. TADs become weaker at the 2-cell stage, followed by gradual consolidation. Compartments A/B are markedly weak in 1-cell SCNT embryos and become increasingly strengthened afterward. By the 8-cell stage, somatic chromatin architecture is largely reset to embryonic patterns. Unexpectedly, we found cohesin represses minor zygotic genome activation (ZGA) genes (2-cell specific genes) in pluripotent and differentiated cells, and pre-depleting cohesin in donor cells facilitates minor ZGA and SCNT. These data reveal multi-step reprogramming of 3D chromatin architecture during SCNT and support dual roles of cohesin in TAD formation and minor ZGA repression.

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RNA-seq of H3.3 knockout and wild type chicken DT40 cells

Project description:RNA-seq was performed for transcriptional analysis of wild-type DT40 cells (Gallus gallus, B-cell line) and a H3.3 knockout line (h3.3a-/-, h3.3b-/-). H3.3 is a H3 histone variant encoded on two genes (H3.3A and H3.3B) in chickens.

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Maternal TDP-43 interacts with RNA Pol II and regulates zygotic genome activation

Project description:Zygotic genome activation (ZGA) is essential for early embryonic development. However, the regulation of ZGA remains elusive in mammals. Here we report that a maternal factor TDP-43, a nuclear transactive response DNA-binding protein, regulates ZGA through RNA Pol II and is essential for mouse early embryogenesis. Maternal TDP-43 translocates from the cytoplasm into the nucleus at the early two-cell stage when minor to major ZGA transition occurs. Genetic deletion of maternal TDP-43 results in mouse early embryos arrested at late two-cell stage and female infertile. TDP-43 co-occupies with RNA Pol II as large foci in the nucleus and also at the promoters of ZGA genes at the late two-cell stage. Biochemical evidence indicates that TDP-43 binds Polr2a and Cyclin T1. Depletion of maternal TDP-43 caused the loss of Pol II foci and reduced Pol II binding on chromatin at major ZGA genes, accompanied by defective ZGA. Collectively, our results suggest that maternal TDP-43 is critical for mouse early embryonic development, in part through facilitating the correct RNA Pol II configuration and zygotic genome activation.

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