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BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ChIP-seq]

ABSTRACT: Post-translational modifications (PTMs) on histones play essential roles in cell fate decisions during development. However, how these PTMs are recognized and coordinated remains to be fully illuminated. Here, we show that BRPF1, a multi-histone binding module protein, is essential to maintain pluripotency in human embryonic stem cells (ESCs). BRPF1, H3K4me3 and H3K23ac substantially co-occupy the active and stemness genes in hESCs. BRPF1 deletion impairs H3K23ac and leads to pluripotency exit and closed chromatin accessibility on stemness genes. Deletion of the N terminal or PHD-zinc knuckle-PHD (PZP) modules completely impairs BRPF1 to maintain hESC pluripotency while PWWP module deletion only partially impact its functions. Together, we reveal that the multi-histone binding module protein, BRPF1 co-ordinates the crosstalk between different histone modifications to maintain the pluripotency in hESCs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE213692 | GEO | 2022/12/21

REPOSITORIES: GEO

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BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

Project description:Post-translational modifications (PTMs) on histones play essential roles in cell fate decisions during development. However, how these PTMs are recognized and coordinated remains to be fully illuminated. Here, we show that BRPF1, a multi-histone binding module protein, is essential to maintain pluripotency in human embryonic stem cells (ESCs). BRPF1, H3K4me3 and H3K23ac substantially co-occupy the active and stemness genes in hESCs. BRPF1 deletion impairs H3K23ac and leads to pluripotency exit and closed chromatin accessibility on stemness genes. Deletion of the N terminal or PHD-zinc knuckle-PHD (PZP) modules completely impairs BRPF1 to maintain hESC pluripotency while PWWP module deletion only partially impact its functions. Together, we reveal that the multi-histone binding module protein, BRPF1 co-ordinates the crosstalk between different histone modifications to maintain the pluripotency in hESCs.

2022-12-21 | GSE213694 | GEO

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ATAC-seq]

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The functional role of OGDH for maintaining mitochondrial respiration and identity of primed human embryonic stem cells

Project description:Human embryonic stem cells (hESCs) can self-renew infinitely or differentiate into the 3 germ layer lineages in vitro with certain cues, holding great promise to model early human embryo development ex vivo. It is wildly accepted that hESCs take advantage of both glycolysis and mitochondrial respiration to favor the naïve pluripotency, while prefer glycolysis to support the primed pluripotency. Thus, the function of mitochondrial respiration in primed hESCs has been underestimated for a long time, and has not been fully understood yet. Herein, we report that the adenosine triphosphate (ATP) production rate is comparable between mitochondrial respiration and glycolysis, suggesting that mitoATP may serve as one of the major sources of the ATP pool in primed hESCs. To further reveal the function of mitochondrial respiration, we deployed inducible CRISPRi method to inhibit OGDH expression with high efficiency, resulting in the TCA cycle blockade as well as the diminishment of mitochondrial respiration activity and total ATP level. Of note, OGDH deficiency led to the exit of primed pluripotency accompanied by cell death. Furthermore, the treatment with small molecule inhibitors to block electron transport chain (ETC) can phenocopy the loss-of-function of OGDH in hESCs. Therefore, genetic and pharmacological perturbations on mitochondrial respiration can impair the stemness of primed hESCs. Collectively, the current study unveils that OGDH acts as a key regulator to fine-tune the abundance of TCA cycle metabolites to ensure the mitochondrial respiration activity in primed hESCs, and highlights the pivotal roles of mitochondrial respiration in terms of ATP production and the maintenance of primed pluripotency. Our findings may provide insights into the linkage between pluripotent states and energy metabolism in hESCs.

2022-03-03 | MTBLS4223 | MetaboLights

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency

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Deciphering a distinct regulatory network of TEAD4, CDX2 and GATA3 in humans for trophoblast transition from embryonic stem cells

Project description:In this study, we perform multiple gain- and loss-of-function of TEAD4, CDX2 or GATA3 to study their roles in the trophoblast transition from BMP4-treated human embryonic stem cells (hESCs). Although hESCs with TEAD4 deletion maintain in pluripotency, their potential of trophoblast transition is attenuate. We then performed large-scale transcriptome analysis to explore more information.

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Multivalent histone and DNA engagement by the triple reader module of ZMYND8 directs the recruitment of a transcriptional network to genes to regulate gene expression

Project description:Elucidation of multivalent interactions involving both DNA and histone post-translational-modifications (PTMs) is essential for providing insight into complex biological functions. We report here the high resolution crystal structure of the N-terminal triple reader module (PHD-Bromo-PWWP) of ZMYND8, which forms a stable unit, capable of simultaneously recognizing histone PTMs and providing a charged platform for DNA interaction. Monte Carlo simulations provide a model whereby the reader module directly engages the core nucleosome particle, extracting the entire histone H3 tail and initiating contacts with the DNA super-coil structure. Systematic mutation of these interaction interfaces reveals cooperativity within the ensemble. Single domain disruption destroys the functional network of interactions initiated by ZMYND8, which impairs recruitment to sites of DNA damage and alters transcription. Taken together, our results establish an important role of the ZMYND8 multivalent reader module in nucleosome binding and chromatin function.

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BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ChIP-seq]

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ChIP-seq]

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BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

| PRJNA882080 | ENA

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ATAC-seq]

Project description:BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [ATAC-seq]

| PRJNA882078 | ENA

ELABELA Is an Endogenous Growth Factor that Sustains hESC Self-Renewal Via the PI3K/AKT Pathway

Project description:ELABELA (ELA) is a peptide hormone required for heart development that signals via the Apelin Receptor (APLNR, APJ). ELA is also abundantly secreted by human embryonic stem cells (hESCs), which do not express APLNR. Here we show that ELA signals in a paracrine fashion in hESCs to maintain self-renewal. ELA inhibition by CRISPR/Cas9-mediated deletion, shRNA or neutralizing antibodies causes reduced hESC growth, cell death and loss of pluripotency. Global phosphoproteomic and transcriptomic analyses of ELA-pulsed hESCs show that it activates PI3K/AKT/mTORC1 signaling required for cell survival. ELA promotes hESC cell cycle progression and protein translation, and blocks stress-induced apoptosis. INSULIN and ELA have partially overlapping functions in hESC medium, but only ELA can potentiate the TGFβ pathway to prime hESCs towards the endoderm lineage. We propose that ELA, acting through an alternate cell-surface receptor, is an endogenous secreted growth factor in human embryos and hESCs that promotes growth and pluripotency. Global Transcriptomic Analysis of INSULIN versus ELA-pulsed human embryonic stem cells was performed to elucidate the functional overlap between these two ligands

2015-09-20 | E-GEOD-71949 | biostudies-arrayexpress

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