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Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [ChIP-seq]

ABSTRACT: Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [ChIP-seq]

PROVIDER: PRJNA868744 | ENA |

REPOSITORIES: ENA

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Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs

Project description:Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs

| PRJNA868743 | ENA

Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [RNA-seq]

Project description:The mechanisms by which epigenetic modifications are established in gene regulatory regions of active genes remain elusive. The data presented show that the establishment and recycling of a major epigenetic mark, the acetylated form of the replacement histone H2A.Z, is regulated by cell cycle-specific long noncoding RNAs encoded in regions adjacent to the promoters of active genes. These transcripts, termed SPEARs (S Phase EArly RNAs), are induced in early S phase: their expression precedes that of the downstream genes on which they exert their regulatory action. SPEARs drive the modification and deposition of the acetylated form of histone H2A.Z by bringing together the replacement histone and the histone acetyl transferase TIP60. This widespread bimodal pathway constitutes a novel RNA-mediated mechanism for the establishment of epigenetic marks and cell-specific epigenetic profiles, thereby providing a unifying explanation for the accuracy and persistence of epigenetic marks on chromatin.

2025-08-01 | GSE211057 | GEO

Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [RIP-seq]

2025-08-01 | GSE211056 | GEO

Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [ChIP-seq]

2025-08-01 | GSE211055 | GEO

Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [RNA-seq]

Project description:Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [RNA-seq]

| PRJNA868745 | ENA

Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [RIP-seq]

Project description:Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs [RIP-seq]

| PRJNA868746 | ENA

Formation of an active epigenetic mark and its recycling is mediated by cell cycle-specific RNAs

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

2025-08-01 | GSE211058 | GEO

Repressive and active histone methylation mark distinct promoters in human and mouse spermatozoa

Project description:This SuperSeries is composed of the following subset Series: GSE13863: Repressive and active histone methylation mark distinct promoters in human and mouse spermatozoa (Nimblegen) GSE19889: Repressive and active histone methylation mark distinct promoters in human and mouse spermatozoa (Illumina) Refer to individual Series

2010-05-16 | E-GEOD-19892 | biostudies-arrayexpress

Phosphorylated MED1 Links Transcription Recycling and Cancer Growth

Project description:Mammalian RNA polymerase II (Pol II) initiation, elongation, termination and reinitiation are well studied, but how Pol II dynamically recycles after the transcription cycle remains unclear. By establishing in vitro and in vivo transcription recycling systems, we find that human Mediator 1 (MED1), when phosphorylated at the mammal-specific threonine 1032 by cyclin-dependent kinase 9, dynamically travels with Pol II throughout the transcribed genes to drive Pol II recycling. Mechanistically, MED1 phosphorylation leads to an increase of recycled Pol II via the molecular bridge of MED31, enhancing mRNA output during the transcription recycling process. Importantly, MED1 phosphorylation increases during prostate cancer progression to the lethal phase, and pharmacological inhibition of CDK9 decreases prostate tumor growth through decreasing MED1 phosphorylation and Pol II recycling. Our findings reveal essential mechanisms underlying Pol II recycling and suggest a neglected, yet fundamental Pol II transcription process for therapeutic intervention.

2022-04-20 | GSE127894 | GEO

Ascorbic acid reprogrames epigenome and epitranscriptome by recycling Fe (III) into Fe (II) in the catalytic cycle of dioxygenases (m6A)

Project description:Ascorbic acid has been reported to stimulate DNA iterative oxidase TET enzymes, Jumonji C-domain-containinghistone demethylase and potentially RNA m6A demethylase FTO and ALKBH5 as a cofactor. Although ascorbic acid has been widely investigated in reprogramming DNA and histone methylation status in vitro, in cell lines and mouse models, its specific role in the catalytic cycle of dioxygenases remains enigmatic. Here we systematically investigated the stimulation of ascorbic towards TET2, ALKBH3, histone demethylases and FTO. We find that ascorbic acid reprograms epitranscrip-tome by erasing the hypermethylated m6A sites. Biochemistry and Electron spin resonance (ESR) assays demonstrate that ascorbic acid enters the active pocket of dioxygenases, reduces Fe (III), either incorporated upon protein synthesis or generated upon rebounding the hydroxyl radical during oxidation, into Fe (II). Finally, we propose a new model for the catalytic cycle of dioxygenases by adding in the essential dynamic cofactor, ascorbic acid. Ascorbic acid refreshes and regenerates inactive dioxygenase through recycling Fe (III) into Fe (II) in a dynamic “hit-and-run” manner.

2024-02-01 | GSE242758 | GEO

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