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Nelfb promotes dWAT formation through RNA Polymerase II-mediated adipogenic gene regulation

ABSTRACT: Nelfb promotes dWAT formation through RNA Polymerase II-mediated adipogenic gene regulation

PROVIDER: PRJNA1231624 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32571112_1.fastq.gz	Fastqsanger.gz
	SRR32571112_2.fastq.gz	Fastqsanger.gz
	SRR32571113_1.fastq.gz	Fastqsanger.gz
	SRR32571113_2.fastq.gz	Fastqsanger.gz
	SRR32571114_1.fastq.gz	Fastqsanger.gz

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Nelfb promotes dWAT formation through RNA Polymerase II-mediated adipogenic gene regulation

Project description:Deletion of Nelfb in preadipocyte lineages in mice cause failure in dWAT and other fat depot formation, perinatal lethality, and reduced expression of adipogenic genes

2025-03-07 | GSE291112 | GEO

Polycomb Protein Ezh1 Promotes RNA Polymerase II Elongation

Project description:Polycomb group (PcG) proteins initiate the formation of repressed chromatin domains and regulate developmental gene expression. A mammalian PcG protein, Enhancer of Zeste homolog 2 (Ezh2), triggers transcriptional repression by catalyzing the addition of methyl groups onto lysine-27 of histone H3 (H3K27me2/3)1. This action facilitates the binding of other PcG proteins to histone H3 and compaction of chromatin. Interestingly, there exists a paralog of Ezh2, termed Ezh1, whose primary function remains unclear. Here, we provide evidence for genome-wide association of Ezh1 with active epigenetic marks, RNA polymerase II (PolII) and mRNA production. Ezh1 depletion reduced global PolII occupancy within gene bodies and resulted in delayed transcriptional activation during differentiation of skeletal muscle cells. Conversely, ectopic expression of wild-type Ezh1 led to premature gene activation and rescued PolII-elongation defects in Ezh1-depleted cells. Collectively, these findings reveal an unanticipated role of a PcG protein in promoting mRNA transcription. Examination of 3 different histone modifications, 3 modified forms of RNA polymerase II, Ezh1, Ezh2 and mRNA levels in a skeletal muscle cells at various developmental stages.

2011-11-23 | E-GEOD-25549 | biostudies-arrayexpress

Senataxin Promotes RNA Polymerase II Elongation [TTseq]

Project description:Senataxin Promotes RNA Polymerase II Elongation [TTseq]

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Senataxin Promotes RNA Polymerase II Elongation [RChIPseq]

Project description:Senataxin Promotes RNA Polymerase II Elongation [RChIPseq]

| PRJNA1175733 | ENA

Senataxin Promotes RNA Polymerase II Elongation [DRBrelease_TTseq]

Project description:Senataxin Promotes RNA Polymerase II Elongation [DRBrelease_TTseq]

| PRJNA1175735 | ENA

Senataxin Promotes RNA Polymerase II Elongation [Hap1_DRBrelease_TTseq]

Project description:Senataxin Promotes RNA Polymerase II Elongation [Hap1_DRBrelease_TTseq]

| PRJNA1262997 | ENA

Senataxin Promotes RNA Polymerase II Elongation [Hap1_TTseq]

Project description:Senataxin Promotes RNA Polymerase II Elongation [Hap1_TTseq]

| PRJNA1262998 | ENA

Senataxin Promotes RNA Polymerase II Elongation [PROseq]

Project description:Senataxin Promotes RNA Polymerase II Elongation [PROseq]

| PRJNA1175732 | ENA

Pausing of RNA polymerase II disrupts DNA-specified nucleosome organization to enable precise gene regulation: Expression data

Project description:Metazoan transcription is controlled through either coordinated recruitment of transcription machinery to the gene promoter, or subsequently, through regulated pausing of RNA polymerase II (Pol II) in early elongation. We report that a key difference between genes that use these distinct regulatory strategies lies in the chromatin architecture specified by their DNA sequences. Pol II pausing is prominent at highly-regulated genes whose sequences inherently disfavor nucleosome formation within the gene, but favor nucleosomal occlusion of the promoter. Pausing of polymerase maintains these genes in an active state by inhibiting the formation of repressive promoter chromatin. In contrast, promoters of housekeeping genes that lack paused Pol II are deprived of nucleosomes regardless of polymerase binding, but show higher nucleosome occupancy downstream. Our results suggest that the “default” chromatin state of a gene instructs its regulation, and that highly-regulated promoters have evolved to encourage competition between nucleosomes and paused Pol II for promoter occupancy.

2010-10-18 | GSE24133 | GEO

Pausing of RNA polymerase II disrupts DNA-specified nucleosome organization to enable precise gene regulation: ChIP-chip data

Project description:Metazoan transcription is controlled through either coordinated recruitment of transcription machinery to the gene promoter, or subsequently, through regulated pausing of RNA polymerase II (Pol II) in early elongation. We report that a key difference between genes that use these distinct regulatory strategies lies in the chromatin architecture specified by their DNA sequences. Pol II pausing is prominent at highly-regulated genes whose sequences inherently disfavor nucleosome formation within the gene, but favor nucleosomal occlusion of the promoter. Pausing of polymerase maintains these genes in an active state by inhibiting the formation of repressive promoter chromatin. In contrast, promoters of housekeeping genes that lack paused Pol II are deprived of nucleosomes regardless of polymerase binding, but show higher nucleosome occupancy downstream. Our results suggest that the âdefaultâ chromatin state of a gene instructs its regulation, and that highly-regulated promoters have evolved to encourage competition between nucleosomes and paused Pol II for promoter occupancy. All experiments were done using two channels per chip, comparing DNA immunoprecipitated by the indicated antibody to matching input chromatin used for affinity purification. Where appropriate, replicate data sets were averaged.

2010-10-18 | E-GEOD-20471 | biostudies-arrayexpress

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