Nucleation-dependent propagation of Polycomb modifications emerges during the Drosophila maternal to zygotic transition
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PROVIDER: PRJNA1273894 | ENA |
REPOSITORIES: ENA
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Project description:The manuscript associated with these datasets seeks to address the timing of acquisition of chromatin modifications associated with Polycomb group (PcG) function during the maternal-to-zygotic transition of Drosophila melanogaster. PcG modifications including mono- and tri-methylation of Histone H3 at Lysine 27 (H3K27me1, me3) and ubiquitylation of H2A at lysine 118 (H2Aub) were measured by ChIP-seq in precisely staged embryo collections spanning large scale zygotic genome activation (ZGA), over nuclear divisions NC13 and three timepoints in NC14 (NC14-early, -mid, and -late). Additionally, marks associated with active transcription, including mono- di- and tri-methylation of Histone H3 at Lysine 4 (H3K4me1, me2, me3), RNA Pol2 phosphorylated at serine 5 of the C-terminal domain heptapeptide repeats, and acetylation of Histone H3 at Lysine 27 (H3K27ac) were measured at NC14. We additionally measured genomic localization of the H3K27me3 methyltransferase, Enhancer of zeste (E(z)), and of three factors known to bind Polycomb Response Elements, Pho, Combgap, and GAGA-Factor (GAF), by generating GFP chimeras to these proteins using CRISPR/Cas9 and performing ChIP against the GFP tagged proteins. Data for these GFP-ChIP-seq localization experiments is from embryos collected during NC14. To test for the contribution of DNA binding factors to the establishment of PcG modifications, we additionally measured deposition of H3K27me3 in embryos where GAF was sequestered from nuclei using Jabba Trap (JT-GAF), and measured H3K27me3, H2Aub, E(z), and RNA Pol2 in embryos from zelda mutant germline clones staged at mid-NC14. Negative control ChIP-seq datasets are provided in the form of anti-GFP ChIP in wild-type embryos that express no GFP tagged protein.
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Project description:Nucleation and spreading of H3K27me3 are critical steps for the initiation and maintenance, respectively, of mitotically inheritable Polycomb-mediated repressive chromatin states in cell identity memory, in both animals and plants. Although a semiconservative read-and-write mechanism is proposed to play a key role in H3K27me3 propagation, the specific determinant and underlying mechanism by which the Polycomb Repressive Complex 2 (PRC2) accesses unmodified nucleosomes for propagating H3K27me3 remain enigmatic. Using Arabidopsis thaliana as a model, we show that the chromatin remodeling activity of PICKLE (PKL) has a specialized role in H3K27me3 spreading to safeguard cell identity during differentiation. PKL specifically binds to H3K27me3 spreading regions but not nucleation sites of Polycomb target genes and physically interacts with the MSI1 subunit of PRC2. Loss of PKL abolishes the occupancy of the PRC2 catalytic subunit CLF in spreading regions and leads to aberrant differentiation. Nucleosome condensing endowed by the ATPase function of PKL ensures that unmodified nucleosomes are accessible to PRC2 catalytic activity. Our findings highlight that PKL-dependent nucleosome compaction is critical for PRC2-mediated H3K27me3 read-and-write functions in H3K27me3 spreading, thus revealing a mechanism by which repressive chromatin domains are established and propagated.
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Project description:Nucleation and spreading of H3K27me3 are critical steps for the initiation and maintenance, respectively, of mitotically inheritable Polycomb-mediated repressive chromatin states in cell identity memory, in both animals and plants. Although a semiconservative read-and-write mechanism is proposed to play a key role in H3K27me3 propagation, the specific determinant and underlying mechanism by which the Polycomb Repressive Complex 2 (PRC2) accesses unmodified nucleosomes for propagating H3K27me3 remain enigmatic. Using Arabidopsis thaliana as a model, we show that the chromatin remodeling activity of PICKLE (PKL) has a specialized role in H3K27me3 spreading to safeguard cell identity during differentiation. PKL specifically binds to H3K27me3 spreading regions but not nucleation sites of Polycomb target genes and physically interacts with the MSI1 subunit of PRC2. Loss of PKL abolishes the occupancy of the PRC2 catalytic subunit CLF in spreading regions and leads to aberrant differentiation. Nucleosome condensing endowed by the ATPase function of PKL ensures that unmodified nucleosomes are accessible to PRC2 catalytic activity. Our findings highlight that PKL-dependent nucleosome compaction is critical for PRC2-mediated H3K27me3 read-and-write functions in H3K27me3 spreading, thus revealing a mechanism by which repressive chromatin domains are established and propagated.
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Project description:Epigenetic inheritance of gene expression states enables a single genome to maintain distinct cellular identities. How histone modifications contribute to this process remains unclear. Using global chromatin perturbations and local, time-controlled modulation of transcription, we establish the existence of epigenetic memory of transcriptional activation for genes that can be silenced by the Polycomb group. This property emerges during cell differentiation and allows genes to be stably switched following a transient transcriptional stimulus. This transcriptional memory state at Polycomb targets operates in cis; however, rather than relying solely on read-and-write propagation of histone modifications, the memory is also linked to the strength of activating input opposing Polycomb proteins and therefore varies with the cellular context. Our data and computational simulations suggest a model whereby transcriptional memory arises from double-negative feedback between Polycomb-mediated silencing and active transcription. Epigenetic memory at Polycomb targets thus depends not only on histone modifications but also on the gene-regulatory network and underlying identity of a cell.
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Project description:Epigenetic inheritance of gene expression states enables a single genome to maintain distinct cellular identities. How histone modifications contribute to this process remains unclear. Using global chromatin perturbations and local, time-controlled modulation of transcription, we establish the existence of epigenetic memory of transcriptional activation for genes that can be silenced by the Polycomb group. This property emerges during cell differentiation and allows genes to be stably switched following a transient transcriptional stimulus. This transcriptional memory state at Polycomb targets operates in cis; however, rather than relying solely on read-and-write propagation of histone modifications, the memory is also linked to the strength of activating input opposing Polycomb proteins and therefore varies with the cellular context. Our data and computational simulations suggest a model whereby transcriptional memory arises from double-negative feedback between Polycomb-mediated silencing and active transcription. Epigenetic memory at Polycomb targets thus depends not only on histone modifications but also on the gene-regulatory network and underlying identity of a cell.
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