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Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [RNA-seq]

ABSTRACT: Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [RNA-seq]

PROVIDER: PRJNA1055017 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27297079.fastq.gz	Fastqsanger.gz
	SRR27297080.fastq.gz	Fastqsanger.gz
	SRR27297081.fastq.gz	Fastqsanger.gz
	SRR27297082.fastq.gz	Fastqsanger.gz
	SRR27297083.fastq.gz	Fastqsanger.gz

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Altered cofactor recruitment and nucleosome dynamics underlie bisphenol A's impact on ERα-mediated transcriptional bursting

Project description:Altered cofactor recruitment and nucleosome dynamics underlie bisphenol A's impact on ERα-mediated transcriptional bursting

| PRJNA1055009 | ENA

Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [ATAC-seq]

Project description:Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [ATAC-seq]

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Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [CUT&Tag]

Project description:Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [CUT&Tag]

| PRJNA1055019 | ENA

Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [RNA-seq]

Project description:Gene regulation is complex, involving the coordination of hundreds of proteins to initiate transcription. At individual loci, transcriptional initiation is stochastic, resulting in short periods of nascent RNA synthesis known as transcriptional bursts. To understand how altered Estrogen Receptor α (ERα) function and cofactor recruitment regulates transcriptional bursting, we utilized single molecule imaging of estrogen responsive genes in Bisphenol A (BPA) treated cells. We observe that cells treated with BPA exhibited TFF1 burst initiation rates and sizes which were indistinguishable from cells induced with Estradiol (E2). However, we observed a 50% reduction in the number of active alleles in BPA treated cells. This effect is gene specific, as GREB1 was unperturbed. Although we observed no difference in chromatin accessibility, the TFF1 promoter exhibited an altered structure which coincided with reduced ERα and cofactor binding. Lastly, deletion of the enhancer locus removed the BPA effect, indicating that enhancer function was perturbed. Our results demonstrate gene specific effects of altered ERα recruitment and function which lead to a reduction of transcriptionally permissive states. Our work supports the model that the initial estrogen response occurs from alleles in primed transcriptionally permissive states with additional inactive alleles contributing to the cellular response over time.

2025-06-02 | GSE251651 | GEO

Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [ATAC-seq]

2025-06-02 | GSE251650 | GEO

Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [CUT&Tag]

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Altered cofactor recruitment and nucleosome dynamics underlie bisphenol A's impact on ERα-mediated transcriptional bursting.

Project description: Not available

| S-EPMC12268693 | biostudies-literature

Altered cofactor recruitment and nucleosome dynamics underlie bisphenol A's impact on ERα-mediated transcriptional bursting

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

2025-06-02 | GSE251654 | GEO

Regulation of stochastic gene bursting by chromatin-independent acetylation

Project description:Stochastic transcriptional bursting is now recognized as a universal property of gene expression. While different genes exhibit distinct bursting patterns, the molecular basis for differences in bursting are largely unknown. We have developed and applied a high-throughput-imaging based screening strategy to identify cellular factors and mechanisms that determine the bursting behavior of human genes. Focusing on epigenetic regulators, we find that global acetylation is the strongest acute modulator of burst frequency, size and heterogeneity of bursting. Acetylation similarly affected the Off-time but On-time changes were gene-specific. These effects were not strongly linked to promoter acetylation, which did not correlate with bursting properties and forced promoter acetylation altered bursting for only some genes. Instead, we identified acetylation of the Integrator complex as a key determinant of gene bursting with elevated Integrator acetylation leading to faster bursting. Taken together our results suggest a dominant role of non-histone proteins in determining gene bursting properties and they identify non-epigenetic acetylation of a transcription cofactor as an allosteric modulator of bursting via a pause-release related bursting checkpoint

2024-06-26 | GSE254866 | GEO

Regulation of stochastic gene bursting by chromatin-independent acetylation

Project description:Stochastic transcriptional bursting is a universal property of gene expression. Different genes exhibit distinct bursting patterns, but the molecular mechanisms that determine bursting kinetics are largely unknown. We have developed and applied a high-throughput-imaging based screening strategy to identify cellular factors and mechanisms that determine the bursting behavior of human genes. Focusing on epigenetic regulators, we find that protein acetylation is a strong acute modulator of burst frequency, burst size and heterogeneity of bursting. Acetylation globally affected the Off-time of genes, but had gene-specific effects on the On-time. Yet, these effects were not linked to promoter acetylation, which did not correlate with bursting properties, and forced promoter acetylation had variable effects on bursting. Instead, we identified acetylation of the Integrator complex as a key determinant of gene bursting. Specifically, we find that elevated Integrator acetylation increases bursting. Taken together our results suggest a prominent role of non-histone proteins in determining gene bursting properties, and they point towards histone-independent acetylation of a transcription cofactor as an allosteric modulator of bursting via a pause-release related bursting checkpoint.

2024-04-24 | MSV000094611 | MassIVE

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