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‘Placeholder’ nucleosomes underlie germline-to-embryo DNA methylation reprogramming [ChIP-Seq]

ABSTRACT: The function and retention/reprogramming of epigenetic marks during the germline-to-embryo transition is a key issue in developmental and cellular biology, with relevance to stem cell programming and trans-generational inheritance. In zebrafish, DNAme patterns are programmed in transcriptionally-quiescent early cleavage embryos; paternally-inherited patterns are maintained, whereas maternal patterns are reprogrammed to match the paternal pattern. Here we show that a ‘placeholder’ nucleosome, containing the histone H2A variant H2A.Z(FV) and H3K4me1, occupies virtually all regions lacking DNAme in both sperm and cleavage embryos – residing at promoters encoding housekeeping and early embryonic transcription factors. Upon genome-wide transcriptional onset, genes with the Placeholder become either active H3K4me3-marked or silent H3K4me3/K27me3-marked (bivalent). Importantly, functional perturbation causing Placeholder loss confers DNAme acquisition, whereas acquisition/expansion of Placeholder confers DNA hypomethylation and improper gene activation. Thus, during transcriptionally quiescent stages (gamete-zygote-cleavage), an H2A.Z(FV)/H3K4me1-containing Placeholder nucleosome deters DNAme, poising parental genes for either gene-specific activation or facultative repression.

ORGANISM(S): Danio rerio

PROVIDER: GSE95030 | GEO | 2017/12/12

SECONDARY ACCESSION(S): PRJNA375789

REPOSITORIES: GEO

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‘Placeholder’ nucleosomes underlie germline-to-embryo DNA methylation reprogramming [RNA-Seq]

Project description:The function and retention/reprogramming of epigenetic marks during the germline-to-embryo transition is a key issue in developmental and cellular biology, with relevance to stem cell programming and trans-generational inheritance. In zebrafish, DNAme patterns are programmed in transcriptionally-quiescent early cleavage embryos; paternally-inherited patterns are maintained, whereas maternal patterns are reprogrammed to match the paternal pattern. Here we show that a ‘placeholder’ nucleosome, containing the histone H2A variant H2A.Z(FV) and H3K4me1, occupies virtually all regions lacking DNAme in both sperm and cleavage embryos – residing at promoters encoding housekeeping and early embryonic transcription factors. Upon genome-wide transcriptional onset, genes with the Placeholder become either active H3K4me3-marked or silent H3K4me3/K27me3-marked (bivalent). Importantly, functional perturbation causing Placeholder loss confers DNAme acquisition, whereas acquisition/expansion of Placeholder confers DNA hypomethylation and improper gene activation. Thus, during transcriptionally quiescent stages (gamete-zygote-cleavage), an H2A.Z(FV)/H3K4me1-containing Placeholder nucleosome deters DNAme, poising parental genes for either gene-specific activation or facultative repression.

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

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NSD1-deposited H3K36me2 directs de novo methylation in the mouse male germline and counteracts Polycomb-associated silencing

Project description:While de novo DNA methylation (DNAme) in mammalian germ cells is dependent upon DNMT3A and DNMT3L, oocytes and spermatozoa show distinct patterns of DNAme. In mouse oocytes, de novo DNAme requires the lysine methyltransferase (KMTase) SETD2, which deposits H3K36me3. Surprisingly, we show here that SETD2 is dispensable for de novo DNAme in the male germline. Rather, the KMTase NSD1, which broadly deposits H3K36me2 in euchromatic regions, plays a critical role in de novo DNAme in prospermatogonia, including of imprinted genes. However, males deficient in germline NSD1 show a more severe defect in spermatogenesis than Dnmt3l-/- males. Furthermore, unlike DNMT3L, NSD1 safeguards a subset of genes against H3K27me3-associated transcriptional silencing. In contrast, H3K36me2 plays only a minor role in de novo DNAme during oogenesis and females with NSD1 deficient oocytes are fertile. Thus, the sexually dimorphic pattern of DNAme in mature mouse gametes is driven by distinct profiles of H3K36 methylation.

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Project description:Placeholder

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Maternal DNMT3A-dependent de novo methylation of the zygotic paternal genome inhibits gene expression in the early embryo

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2020-08-19 | GSE141877 | GEO

Food vacuole proteome of P. berghei heme pathway ferrochelatase knockout parasite by LC-MS/MS

Project description:LC-MS/MS of in-solution trypsin digested FV protein extracts was carried out for the FVs isolated from PbWT and PbFCKO parasites. The FV preparations had signature FV proteins such as plasmepsin IV, berghepain, aminopeptidases, subunits of vacuolar-type H+ATPase (V-type H ATPase), together with parasitophorous vacuolar (PV) proteins including exported protein 1 (Exp1), Exp2, early transcribed membrane protein, PV1, PV5 (lipocalin) etc., and Rab GTPases associated with cytostome-FV trafficking. A total number of 251 and 201 proteins could be identified for WT (P1) and FCKO (P2) FVs, respectively, and 175 proteins were common between them suggesting an overall consistency in the preparations. The results obtained have suggested that the FV proteome in FCKO parasites is compromised. None of the subunits of V-type H+ATPase - a proton pump maintaining the acidic pH of FV could be detected in FCKO FVs indicating the lower abundance of these proteins. In addition, berghepain-2 - a cysteine protease involved in Hb degradation could not be detected in FCKO FVs.

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