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The H3K4me1 plays a role in nucleosome depletion at enhancers but does not directly contribute to eRNA synthesis. [RNA-Seq]

ABSTRACT: We found that H3K4me1 contributes to nucleosome depletion at enhancers but was not enhough for eRNA synthesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147825 | GEO | 2021/07/14

REPOSITORIES: GEO

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The H3K4me1 plays a role in nucleosome depletion at enhancers but does not directly contribute to eRNA synthesis. [RNA-Seq]

Project description:The H3K4me1 plays a role in nucleosome depletion at enhancers but does not directly contribute to eRNA synthesis. [RNA-Seq]

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Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers [ChIP-seq_2]

Project description:We found that H3K4me1 contributes to nucleosome depletion at enhancers but was not enhough for eRNA synthesis.

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Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers. [ChIP-Seq]

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Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers

Project description:Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers

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Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers. [ChIP-Seq]

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Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers [ChIP-seq_2]

Project description:Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers [ChIP-seq_2]

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Histone H3K4me1 and H3K27ac play roles in nucleosome depletion and eRNA transcription, respectively, at enhancers

Project description:This SuperSeries is composed of the SubSeries listed below.

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Mll3 and Mll4 facilitate enhancer RNA synthesis and transcriptional elongation from promoters independently of H3K4 monomethylation

Project description:Monomethylation of histone H3 at lysine 4 (H3K4me1) and acetylation of histone H3 at lysine 27 (H3K27ac) are correlated with transcriptionally engaged enhancer elements, but the functional impact of these modifications on enhancer activity is not well understood. Here we used CRISPR/Cas9 genome editing to separate catalytic activity-dependent and independent functions of Mll3 (Kmt2c) and Mll4 (Kmt2d, Mll2), the major enhancer H3K4 monomethyltransferases. Loss of Mll3/4 catalytic activity and H3K4me1 from enhancers causes partial depletion of H3K27ac, but surprisingly minor effects on enhancer Pol II binding, enhancer RNA (eRNA) transcription and gene expression. In contrast, loss of Mll3/4 proteins results in dramatic reduction of eRNA production, concomitant with impaired transcriptional elongation at adjacent promoters. Altogether our results suggest the major coactivator function of Mll3/4 is largely independent of H3K4me1 and instead linked to enhancer Pol II occupancy, eRNA transcription and long-range influence on elongation at target promoters.

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H3K4me1 directs H3K36me2 and H3K36me3 deposition in land plants

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Project description:The evidence that several signal and ligand-dependent pathways function by activating regulatory enhancer programs suggests that a “checkpoint” strategy may underline activation of some or even many diversely-regulated enhancers. Here, we report a molecular mechanism common to several acute signal- and ligand-dependent enhancer activation programs based on release of a shared eRNA transcription checkpoint. This requires recruitment of a DNA-PKcs-phosphorylated RING finger repressor, KAP1, functioning as a modulator, inhibiting its association with 7SK and E3 SUMO ligase activity on the CDK9 subunit of P-TEFb, facilitating formation of an activated P-TEFb complex, licensing eRNA elongation. Overcoming this checkpoint for signal-dependent enhancer activation occurs in diverse pathways including estrogen receptor α, NF-κB-regulated proinflammatory, androgen receptor and neuronal depolarization. Therefore, a specific strategy required to convert a basal state enhancer P-TEFb complex to an active state to release a conserved checkpoint is apparently employed by several functionally-important signal/ligand-regulated regulatory enhancers to implement the instructions of endocrine/paracrine system

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