Genome-wide epigenetic reprogramming during chick embryonic development
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ABSTRACT:
PROVIDER: PRJNA1012695 | ENA |
REPOSITORIES: ENA
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Project description:In mice, genome-wide DNA methylation is actively erased at the onset of fertilisation, followed by remethylation in epiblasts after implantation, leading to inactive chromatin formation as a preliminary step to somatic cell differentiation, and then demethylation again during primitive streak formation and the determination of primordial germ cells (PGCs). This sequence of DNA methylation changes is accompanied by dynamic epigenetic reprogramming, including nuclear structure, histone modification, and intranuclear re-localisation of chromosomes, during totipotency acquisition of the fertilised egg and germline development. Here we show that in the avian strain White Leghorn of Gallus gallus domesticus, global reprogramming of DNA methylation and histone modifications, as seen in mice, is induced during primitive streak formation but then reaches an almost basal state in somatic cells during later embryogenesis unlike mice. Avian chromosomes are subdivided into large and genetically less functioning macrochromosomes (MACs) and gene-rich microchromosomes (MICs), of which remarkable karyotypic composition is evolutionarily conserved from cartilaginous fish to reptiles. We found that these MACs undergo reprogramming that involves particularly active DNA demethylation and removal of trimethylation at lysine 9 of histone H3, leading to activation of the MAC-linked HOXA and HOXD gene clusters that control morphogenesis. We show here that the erasure of genome-wide epigenetics may not only have an important function to initiate differentiation into three germ layers via primitive streak formation, as seen in mice but may also provide a basis for the acquisition of new epigenetics required to regulate morphogenesis during late chicken embryonic development.
2024-10-01 | GSE242250 | GEO
Project description:In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes, however the molecular mechanisms of this specificity remain unclear. Here we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in vivo, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long term epigenetic silencing during mammalian development.
2021-04-22 | PXD023974 | Pride
Project description:Sperm contributes genetic and epigenetic information to the embryo to efficiently support development. However, the mechanism underlying such developmental competence remains elusive. Here, we investigated whether all sperm cells have a common epigenetic configuration that primes transcriptional program for embryonic development. We show for the first time that remodelling of histones during spermiogenesis results in the retention of methylated histone H3 at the same genomic location in every sperm cell. This homogeneously methylated fraction of histone H3 in the sperm genome is maintained during early embryonic replication. Such methylated histone fraction resisting postfertilisation reprogramming marks developmental genes whose expression is perturbed upon experimental reduction of histone methylation. A similar homogeneously methylated histone H3 fraction is detected in human sperm. Altogether, we uncover a conserved mechanism of paternal epigenetic information transmission to the embryo through the homogeneous retention of methylated histone in a sperm cells population.
2020-05-29 | PXD012853 | Pride
Project description:Epigenetic regulation of embryonic skin development
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Project description:Type IV collagen is the main component of the basement membrane which gives strength to the blood-gas barrier. In avians the formation of the blood-gas barrier happens rapidly and before hatching. We have performed a microarray expression analysis in late chick lung development and found that COL4A1 and COL4A2 were among the most significantly upregulated genes during the formation of the avian blood-gas barrier. Our study showed that type IV collagen and therefore the basement membrane play fundamental roles in coordinating alveolar morphogenesis. Four developmental stages of chick lung maturation (E14, E15, E16, E18). Three biological replicates per time point.
2015-11-01 | E-GEOD-72385 | biostudies-arrayexpress
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Project description:Cell state evolution underlies tumor development and response to therapy1, but mechanisms specifying cancer cell states and intratumor heterogeneity are incompletely understood. Schwannomas are the most common tumors of the peripheral nervous system and are treated with surgery and ionizing radiation2–5. Schwannomas can oscillate in size for many years after radiotherapy6,7, suggesting treatment may reprogram schwannoma cells or the tumor microenvironment. Here we show epigenetic reprogramming shapes the cellular landscape of schwannomas. We find schwannomas are comprised of 2 molecular groups distinguished by reactivation of neural crest development pathways or misactivation of nerve injury mechanisms that specify cancer cell states and the architecture of the tumor immune microenvironment. Schwannoma molecular groups can arise independently, but ionizing radiation is sufficient for epigenetic reprogramming of neural crest to immune-enriched schwannoma by remodeling chromatin accessibility, gene expression, and metabolism to drive schwannoma cell state evolution and immune cell infiltration. To define functional genomic mechanisms underlying epigenetic reprograming of schwannomas, we develop a technique for simultaneous interrogation of chromatin accessibility and gene expression coupled with genetic and therapeutic perturbations in single-nuclei. Our results elucidate a framework for understanding epigenetic drivers of cancer evolution and establish a paradigm of epigenetic reprograming of cancer in response to radiotherapy.
2023-04-18 | PXD014798 | Pride
Project description:The S2 subunit of infectious bronchitis virus with flag tag was expressed in chick embryonic kidney cells, purified using flag antibody evolving immunoprecipitation, controls using igG antibody, and the resulting peptides or proteins were identified by protein profiling.
2024-04-24 | PXD041764 | JPOST Repository
Project description:The goal of this study was to determine developmental differences in gene expression between left and right ventricle, and to assess the differential effect of altered hemodynamic loading on left and right ventricle. Chick ventricles from different developmental stages were isolated for assessment of normal developmental profiles. Conotruncal banding or partial ligation of the left atrial appendage was performed in ovo at embryonic day 4 and ventricles were isolated at embryonic day 5 (banding) or 8 (ligation) for assessment of altered loading effects.
2012-12-28 | GSE37070 | GEO
Project description:We characterized the proteome of the auditory brainstem of a chick embryo on embryonic day 13, when apoptosis occurs in auditory nuclei. We identified caspase substrates by searching the peptidome for peptides C-terminal to caspase-typical cleavage sites.
2022-04-01 | PXD030697 | Pride