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SP1 antagonizes H3K27me3 to shape chromatin landscapes for RNA polymerase II recruitment during gastrulation [RNA-seq]

ABSTRACT: Following implantation, the epiblast gives rise to three germ layers that form the cellular foundation of the entire body plan. However, how transcription is initiated and regulated at developmental genes during this critical period remains unclear. By analyzing RNA polymerase II (Pol II) occupancy in mouse post-implantation embryos, we found that Pol II occupies nearly half of bivalent promoters, in a temporally ordered, stepwise manner. H3K27me3 is deposited first at developmental genes, followed by the sequential acquisition of H3K4me3 and Pol II. Pol II recruitment is quantitatively modulated by the opposing activities of KMT2B-mediated H3K4me3 and EED-dependent H3K27me3: loss of H3K4me3 impairs Pol II binding, while depletion of H3K27me3 enhances its occupancy and leads to premature gene activation. Notably, the transcription factor SP1 promotes Pol II recruitment by antagonizing H3K27me3 deposition. These in vivo findings shed light on chromatin-based mechanisms that regulate transcriptional activation of developmental genes during early embryogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE269651 | GEO | 2026/03/19

REPOSITORIES: GEO

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Histone modifications and SP1 balance Pol II recruitment at bivalent promoters during gastrulation

Project description:Progressive activation of bivalent genes is crucial for promoting cell differentiation and embryonic development. However, the mechanisms governing RNA polymerase II recruitment at bivalent promoters remain poorly understood. Here, we unveiled the dynamic landscape of Pol II in mouse post-implantation embryos. Our findings indicated that imprinting genes are selectively activated in embryonic and extra-embryonic lineages. Pseudotranscribed genes exhibit significant dynamism across embryonic germ layers, with transcriptional events preceding substantial mRNA production. The recruitment of Pol II to bivalent promoters is synergistically regulated by KMT2B/H3K4me3, EED/H3K27me3, and SP1 in a dose-dependent manner. Specifically, the absence of H3K4me3 and SP1 reduces Pol II recruitment at promoters, while the loss of H3K27me3 increases Pol II occupancy and derepresses developmental gene expression. Our in vivo study not only elucidated the mechanism of Pol II recruitment at bivalent promoters in mammals, but also provided a valuable framework for exploring gene regulation mechanisms in disease contexts.

2026-03-19 | GSE269652 | GEO

Poised RNA Polymerase II changes over developmental time and prepares genes for future expression (ChIP-seq data)

Project description:Poised RNA polymerase II is predominantly found at developmental control genes and is thought to allow their rapid and synchronous induction in response to extracellular signals. How the recruitment of poised RNA Pol II is regulated during development is not known. By isolating muscle tissue from Drosophila embryos at five stages of differentiation, we show that the recruitment of poised Pol II occurs at many genes de novo and this makes them permissive for future gene expression. When compared to other tissues, these changes are stage-specific and not tissue-specific. In contrast, Polycomb group repression is tissue-specific and in combination with Pol II (the balanced state) marks genes with highly dynamic expression. This suggests that poised Pol II is temporally regulated and is held in check in a tissue-specific fashion. We compare our data to mammalian embryonic stem cells and discuss a framework for predicting developmental programs based on chromatin state. ChIP-seq for Pol II, H3K4me3 and H3K27me3 in various Drosophila embryos and tissues

2012-12-20 | E-GEOD-34301 | biostudies-arrayexpress

The Polycomb group mutant esc leads to augmented the levels of paused Pol II in the Drosophila embryo.

Project description:The role of Polycomb group (PcG) was studied on RNA Polymerase II (Pol II) pausing phenomenon. Wild type and Polycomb mutant (esc) embryos were used for ChIP-Seq experiments using Pol II and histone methylation antibodies. Enhanced Pol II occupancy was observed for thousands of genes in esc mutant embryos, including genes not known to be bound by PRC2 or having H3K27me3 associated. Most of these genes exhibit a concomitant reduction in H3K27me3 and increase in H3K4me3 at promoter-proximal regions. Silent genes lacking promoter-associated paused Pol II in wild-type embryos are converted into âpoisedâ genes with paused Pol II in esc mutants. We suggest that this conversion of silent genes into poised genes might render differentiated cell types susceptible to switches in identity in PcG mutants. ChIP-Seq data was generated for antibodies against Pol-II, H3K4me3, H3K27me3 in both wild type and esc mutant Drosophila embryos (0-2hr, 8-12hr, and 18-24hr embryos). In addition GRO-Seq data was generated for 18-24hr esc mutant embryos.

2011-06-14 | E-GEOD-28833 | biostudies-arrayexpress

A comprehensive epigenome map of Plasmodium falciparum reveals unique mechanisms of transcriptional regulation

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Different transcriptional strategies for zygotic genome activation in Drosophila [ChIP-Seq]

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2013-07-26 | E-GEOD-41700 | biostudies-arrayexpress

The Polycomb group mutant esc leads to augmented the levels of paused Pol II in the Drosophila embryo.

2011-06-15 | GSE28833 | GEO

Comparision of Bmi-1, Ring1B, H3K27me3, Ser2 Pol II, Ser 5 Pol II binding on Hox and non-Hox genes

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2014-06-27 | E-GEOD-49181 | biostudies-arrayexpress

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Poised RNA Polymerase II changes over developmental time and prepares genes for future expression (MNase-seq data)

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2012-12-20 | E-GEOD-34283 | biostudies-arrayexpress

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