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Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos [ATAC-seq]

ABSTRACT: Vertebrate embryos achieve developmental competency during zygotic genome activation (ZGA) by establishing chromatin states that silence yet poise developmental genes for subsequent lineage-specific activation. Here, we reveal how developmental gene poising is established de novo in preZGA zebrafish embryos. Poising is established at promoters and enhancers that initially contain open/permissive chromatin with ‘Placeholder’ nucleosomes (bearing H2A.Z, H3K4me1, and H3K27ac), and DNA hypomethylation. Silencing is initiated by the recruitment of Polycomb Repressive Complex 1 (PRC1), and H2Aub1 deposition by catalytic Rnf2 during preZGA and ZGA stages. During postZGA, H2Aub1 enables Aebp2-containing PRC2 recruitment and H3K27me3 deposition. Notably, preventing H2Aub1 (via Rnf2 inhibition) eliminates recruitment of Aebp2-PRC2 and H3K27me3, and elicits transcriptional upregulation of certain developmental genes during ZGA. However, upregulation is independent of H3K27me3 – establishing H2Aub1 as the critical silencing modification at ZGA. Taken together, we reveal the logic and mechanism for establishing poised/silent developmental genes in early vertebrate embryos.

ORGANISM(S): Danio rerio

PROVIDER: GSE168361 | GEO | 2022/01/04

REPOSITORIES: GEO

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Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos [ChIP-seq]

Project description:Vertebrate embryos achieve developmental competency during zygotic genome activation (ZGA) by establishing chromatin states that silence yet poise developmental genes for subsequent lineage-specific activation. Here, we reveal how developmental gene poising is established de novo in preZGA zebrafish embryos. Poising is established at promoters and enhancers that initially contain open/permissive chromatin with ‘Placeholder’ nucleosomes (bearing H2A.Z, H3K4me1, and H3K27ac), and DNA hypomethylation. Silencing is initiated by the recruitment of Polycomb Repressive Complex 1 (PRC1), and H2Aub1 deposition by catalytic Rnf2 during preZGA and ZGA stages. During postZGA, H2Aub1 enables Aebp2-containing PRC2 recruitment and H3K27me3 deposition. Notably, preventing H2Aub1 (via Rnf2 inhibition) eliminates recruitment of Aebp2-PRC2 and H3K27me3, and elicits transcriptional upregulation of certain developmental genes during ZGA. However, upregulation is independent of H3K27me3 – establishing H2Aub1 as the critical silencing modification at ZGA. Taken together, we reveal the logic and mechanism for establishing poised/silent developmental genes in early vertebrate embryos.

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Establishment of Developmental Gene Silencing by Ordered Polycomb Complex Recruitment in Early Zebrafish Embryos [RNA-seq]

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Removal of H2Aub1 by ubiquitin-specific proteases 12 and 13 is required for stable Polycomb-mediated gene repression in Arabidopsis

Project description:Background: Stable gene repression is essential for normal growth and development. Polycomb Repressive Complexes 1 and 2 (PRC1 & PRC2) are involved in this process by establishing monoubiquitinated histone 2A (H2Aub1) and subsequent trimethylation of lysine 27 of histone 3 (H3K27me3). Previous work proposed that H2Aub1 removal by the ubiquitin-specific proteases 12 and 13 (UBP12 & UBP13) is part of the repressive PRC1&2 system, but its functional role remains elusive. Results: We show that UBP12 and UBP13 work together with PRC1, PRC2, and EMF1 to repress genes involved in stimulus response. We found that H2Aub1 is associated with responsiveness, and that it’s only indirectly repressive via PRC2 recruitment. Our analyses also revealed that PR2 targets that do not require PRC1 are pre-repressed. Lastly, we have found that removal of H2Aub1 by UBP12/13 prevents loss of H3K27me3, consistent with our finding that the H3K27me3 demethylase REF6 is enriched at H2Aub1 marked genes. Conclusions: Our data allow us to propose a model in which deposition of H2Aub1 permits recruitment of PRC2 and provides a state that allows for a rapid switch between gene activation and repression. Removal of H2Aub1 by UBP12/13 is required to achieve stable repression.

2020-05-19 | GSE131756 | GEO

PR-DUB preserves Polycomb repression by preventing excessive accumulation of H2Aub1, an antagonist of nucleosome stacking (RNA-Seq)

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PR-DUB preserves Polycomb repression by preventing excessive accumulation of H2Aub1, an antagonist of nucleosome stacking (ChIP-Seq)

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PR-DUB preserves Polycomb repression by preventing excessive accumulation of H2Aub1, an antagonist of nucleosome stacking (ATAC-Seq)

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Project description:The Polycomb repressive complexes PRC1 and PRC2 are key mediators of heritable gene silencing in multicellular organisms. Here we characterize AEBP2, a known PRC2 cofactor which, in vitro, has been shown to stimulate PRC2 activity. We show that AEBP2 localises specifically to PRC2 target loci, including the inactive X chromosome. Proteomic analysis confirms that AEBP2 associates exclusively with PRC2 complexes. However, analysis of embryos homozygous for a targeted mutation of Aebp2 unexpectedly revealed a Trithorax phenotype, normally linked to antagonism of Polycomb function. Consistent with this we observe elevated levels of PRC2 mediated histone H3K27 methylation at target loci in Aebp2 mutant embryonic stem cells. We further demonstrate that mutant ES cells assemble atypical hybrid PRC2 sub-complexes, potentially accounting for enhancement of Polycomb activity, and suggesting that AEBP2 normally plays a role in defining the mutually exclusive composition of PRC2 sub-complexes. H3K27me3, SUZ12, and AEBP2 ChIP-Seq in wild-type and AEBP2 KO mouse ESCs, biological replicates, pre-cleared chromatin as input, additionally FS2 ChIP-Seq in cells with FS2 tagged AEBP2, HiSeq2000

2016-08-02 | E-GEOD-83082 | biostudies-arrayexpress

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes [ChIP-seq]

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2013-09-27 | E-GEOD-42705 | biostudies-arrayexpress

Marking of the genome by H3K4 methylation prior to embryonic gene activation

Project description:Early zebrafish embryo development proceeds first from a maternally transcribed and stored mRNAs, and zygotic gene activation (ZGA) is initiated at the mid-blastula transition (MBT; 1000-cell stage), 3.3 h post-fertilization. Very little is known on how the zygotic genome is programmed for transcriptional activation at the MBT. To start addressing this issue, we have mapped by ChIP-chip genome-wide promoter histone methylation (H3K4me3, H3K9me3, H3K27me3, H3K36me3) and RNA Pol II profiles before ZGA (256-cell stage; 2.5 hpf), during ZGA (MBT; 3.5 hpf)) and after ZGA (Post-MBT; 5.3 hpf) . We used a custom 2.1M probe HD promoter array (Nimblegen) for ChIP and input DNA hybridization. Peak detection was done using MA2C with P=10e-4 as cutoff. ChIP-chip experiments were performed from chromatin prepared by sonication after formaldehyde cross-linking, from embryos are the indicated developmental stages and ChIP DNA was hybridized onto the aforementioned Nimbegen promoter arrays.

2011-12-02 | E-GEOD-27314 | biostudies-arrayexpress

The Polycomb Group protein Rnf2/Ring1b is essential for zebrafish development and cardiogenesis

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