Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384286 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Reprogramming of H3K9me3-dependent heterochromatin during mammalian early embryo development
| PRJNA384149 | ENA
Project description:Reprogramming of H3K9me3-dependent heterochromatin during mammalian early embryo development [ChIP-seq]
| PRJNA384169 | ENA
Project description:Reprogramming of H3K9me3-dependent heterochromatin during mammalian early embryo development [RNA-seq]
| PRJNA384287 | ENA
Project description:H3K9me3-dependent heterochromatin is considered as one of the major barriers for cell fate changes, and must be reprogrammed during fertilization to reactivate highly specialized paternal and maternal genome to establish totipotency. However, the molecular details are lacked for early embryos due to the limited materials. Here we map the genome-wide distribution of H3K9me3 modification in the early embryo as well as in the cell fate determined embryonic tissues after implantation. We find that H3K9me3 exhibits distinct dynamic features in promoters and retro-transposons. Both maternal and paternal genome undergo large scale of H3K9me3 reestablishment after fertilization, and the imbalance of maternal H3K9me3 signal over paternal last until the blastocyst stage. The rebuilding of H3K9me3 on LTR retro-transposons maintains its repression state after the global DNA demethylation, and we further discover that Chaf1a is essential for the establishment of H3K9me3 on LTRs and the loss function of Chaf1a leads to embryo development failure. Finally, we find that lineage specific H3K9me3 is established after lineage commitment in post-implantation embryos. Thus, our data demonstrate that H3K9me3-dependent heterochromatin undergoes dramatic reprogramming during early embryo development and the establishment of H3K9me3 on LTRs is essential for proper embryo development.
2018-04-13 | GSE98149 | GEO
Project description:H3K9me3-dependent heterochromatin is considered as one of the major barriers for cell fate changes, and must be reprogrammed during fertilization to reactivate highly specialized paternal and maternal genome to establish totipotency. However, the molecular details are lacked for early embryos due to the limited materials. Here we map the genome-wide distribution of H3K9me3 modification in the early embryo as well as in the cell fate determined embryonic tissues after implantation. We find that H3K9me3 exhibits distinct dynamic features in promoters and retro-transposons. Both maternal and paternal genome undergo large scale of H3K9me3 reestablishment after fertilization, and the imbalance of maternal H3K9me3 signal over paternal last until the blastocyst stage. The rebuilding of H3K9me3 on LTR retro-transposons maintains its repression state after the global DNA demethylation, and we further discover that Chaf1a is essential for the establishment of H3K9me3 on LTRs and the loss function of Chaf1a leads to embryo development failure. Finally, we find that lineage specific H3K9me3 is established after lineage commitment in post-implantation embryos. Thus, our data demonstrate that H3K9me3-dependent heterochromatin undergoes dramatic reprogramming during early embryo development and the establishment of H3K9me3 on LTRs is essential for proper embryo development.
2018-04-13 | GSE98151 | GEO
Project description:H3K9me3-dependent heterochromatin is considered as one of the major barriers for cell fate changes, and must be reprogrammed during fertilization to reactivate highly specialized paternal and maternal genome to establish totipotency. However, the molecular details are lacked for early embryos due to the limited materials. Here we map the genome-wide distribution of H3K9me3 modification in the early embryo as well as in the cell fate determined embryonic tissues after implantation. We find that H3K9me3 exhibits distinct dynamic features in promoters and retro-transposons. Both maternal and paternal genome undergo large scale of H3K9me3 reestablishment after fertilization, and the imbalance of maternal H3K9me3 signal over paternal last until the blastocyst stage. The rebuilding of H3K9me3 on LTR retro-transposons maintains its repression state after the global DNA demethylation, and we further discover that Chaf1a is essential for the establishment of H3K9me3 on LTRs and the loss function of Chaf1a leads to embryo development failure. Finally, we find that lineage specific H3K9me3 is established after lineage commitment in post-implantation embryos. Thus, our data demonstrate that H3K9me3-dependent heterochromatin undergoes dramatic reprogramming during early embryo development and the establishment of H3K9me3 on LTRs is essential for proper embryo development.
2018-04-13 | GSE98150 | GEO
Project description:H3K9me3-dependent heterochromatin is considered as one of the major barriers for cell fate changes, and must be reprogrammed during fertilization to reactivate highly specialized paternal and maternal genome to establish totipotency. However, the molecular details are lacked for early embryos due to the limited materials. Here we map the genome-wide distribution of H3K9me3 modification in the early embryo as well as in the cell fate determined embryonic tissues after implantation. We find that H3K9me3 exhibits distinct dynamic features in promoters and retro-transposons. Both maternal and paternal genome undergo large scale of H3K9me3 reestablishment after fertilization, and the imbalance of maternal H3K9me3 signal over paternal last until the blastocyst stage. The rebuilding of H3K9me3 on LTR retro-transposons maintains its repression state after the global DNA demethylation, and we further discover that Chaf1a is essential for the establishment of H3K9me3 on LTRs and the loss function of Chaf1a leads to embryo development failure. Finally, we find that lineage specific H3K9me3 is established after lineage commitment in post-implantation embryos. Thus, our data demonstrate that H3K9me3-dependent heterochromatin undergoes dramatic reprogramming during early embryo development and the establishment of H3K9me3 on LTRs is essential for proper embryo development. This SuperSeries is composed of the SubSeries listed below.
2018-04-13 | GSE97778 | GEO
Project description:Reprogramming of H3K9me3-dependent heterochromatin is required for early development. How H3K9me3 is involved in early human development is, however, largely unclear. Here, we resolve the temporal landscape of H3K9me3 during human preimplantation development and its regulation for diverse hominoid-specific retrotransposons. At the 8-cell stage, H3K9me3 reprogramming at hominoid-specific retrotransposons termed SINE-VNTR-Alu (SVA) facilitates interaction between certain promoters and SVA-derived enhancers, facilitating the zygotic genome activation. In trophectoderm, de novo H3K9me3 domains prohibit pluripotent transcription factors from binding on hominoid-specific retrotransposons-derived regulatory elements for inner cell mass (ICM)-specific genes. H3K9me3 re-establishment at SVA elements in ICM is associated with higher transcription of DNA damage repair genes, compared to naïve human pluripotent stem cells. Our data demonstrate that species-specific reorganization of H3K9me3-dependent heterochromatin at hominoid-specific retrotransposons plays important roles during early human development, shedding light on how the epigenetic regulatory network for early development has evolved in mammals.
2022-07-14 | GSE176016 | GEO
Project description:Histone modifications are central to the regulation of all DNA-dependent processes but the repertoire of known modifications is far from complete. Lysine 64 of Histone H3 (H3K64) lies within the globular domain of H3 at a structurally important position within the nucleosome. We identify tri-methylation of H3K64 (H3K64me3) as a modification enriched in pericentric heterochromatin and associated with repeated sequences and transcriptionally inactive genomic regions. Interestingly, the pericentric enrichment of H3K64me3 depends on the Suv39h methyltransferases. Further, we show that this newly identified mark is dynamically regulated during the two major epigenetic reprogramming events in mammals. In primordial germ cells (PGCs) H3K64me3 is present at the time of specification, but disappears transiently during germline reprogramming. In the early mouse embryo it is inherited exclusively through the maternal germline and specifically enriched in heterochromatic regions of the maternal pronucleus. Subsequently the modification is rapidly removed from the maternal chromatin suggesting an important role for H3K64me3 turnover in development. Taken together, our findings firmly establish H3K64me3 as a novel histone modification mark of repressive chromatin, which displays crosstalk to the Suv39 pathway and is dynamically reprogrammed during development. We hypothesize that methylation of this lysine helps to 'secure' the nucleosome and perhaps the surrounding heterochromatin, in an appropriately repressed state during development. Keywords: ChIP-chip, embryonic stem cells, H3K64me3, H3K9me3, heterochromatin ChIP-chip experiments were performed with four independent biological replicates for H3K64me3 and two independent replicates for H3K9me3. For each condition hybridizations include a dye-swap experiment.
2010-05-16 | E-GEOD-16185 | biostudies-arrayexpress
Project description:Chromocenters are established after the 2-cell (2C) stage during mouse embryonic development, but the factors that mediate chromocenter formation remain largely unknown. To identify regulators of 2C heterochromatin establishment, we generated an inducible system to convert embryonic stem cells (ESCs) to 2C-like cells. This conversion is marked by a global reorganization and dispersion of H3K9me3-heterochromatin foci, which are then reversibly formed upon re-entry into pluripotency. Profiling the chromatin-bound proteome (chromatome) by genome capture of ESCs transitioning to 2C-like cells, we uncover chromatin regulators involved in de novo heterochromatin formation. We identified TOPBP1 and investigated its binding partner SMARCAD1. SMARCAD1 and TOPBP1 associate with H3K9me3-heterochromatin in ESCs. Interestingly, the nuclear localization of SMARCAD1 is lost in 2C-like cells. SMARCAD1 or TOPBP1 depletion in mouse embryos lead to developmental arrest, reduction of H3K9me3 and remodeling of heterochromatin foci. Collectively, our findings contribute to comprehending the maintenance of chromocenters during early development.
2023-04-18 | PXD019703 | Pride