Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long noncoding RNA-dependent control of Myc transcriptional bursting [HiC]

ABSTRACT: Genes are transcribed in short periods of activity, called bursts. Bursts are initiated by enhancer-promoter contacts and dynamically controlled by the levels of enhancer- and promoter-produced RNAs through a negative feedback mechanism. Here, by direct visualization of nascent transcripts, we show that chromatin-associated long noncoding RNAs (lncRNAs) contribute to the regulation of transcriptional bursting. We find that production of Pvt1 raises the baseline of RNA concentration in the locus of the Myc proto-oncogene and acts locally and in a dose-dependent manner to decrease the duration of Myc bursting. Premature termination of Pvt1 led to higher Myc expression and transcriptional activities, resulting in increased cellular proliferation and advanced tumor development in autochthonous models of lung cancer. These findings point to a critical lncRNA-mediated mechanism for Myc regulation and suggest a potentially widespread role for lncRNAs in fine-tuning gene expression through local control of transcriptional bursting.

ORGANISM(S): Mus musculus

PROVIDER: GSE306102 | GEO | 2025/08/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Long noncoding RNA-dependent control of Myc transcriptional bursting [ATAC-Seq]

Project description:Genes are transcribed in short periods of activity, called bursts. Bursts are initiated by enhancer-promoter contacts and dynamically controlled by the levels of enhancer- and promoter-produced RNAs through a negative feedback mechanism. Here, by direct visualization of nascent transcripts, we show that chromatin-associated long noncoding RNAs (lncRNAs) contribute to the regulation of transcriptional bursting. We find that production of Pvt1 raises the baseline of RNA concentration in the locus of the Myc proto-oncogene and acts locally and in a dose-dependent manner to decrease the duration of Myc bursting. Premature termination of Pvt1 led to higher Myc expression and transcriptional activities, resulting in increased cellular proliferation and advanced tumor development in autochthonous models of lung cancer. These findings point to a critical lncRNA-mediated mechanism for Myc regulation and suggest a potentially widespread role for lncRNAs in fine-tuning gene expression through local control of transcriptional bursting.

2025-08-22 | GSE306101 | GEO

Long noncoding RNA-dependent control of Myc transcriptional bursting [RNA-Seq]

2025-08-22 | GSE306107 | 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

Genome-wide interference of chromatin architecture and Mediator in transcriptional bursting and gene network regulation

Project description:Gene expression is a stochastic process that occurs in bursts of RNA synthesis. We applied a mathematical model to scRNA-Seq data to infer bursting dynamics transcriptome-wide under multiple perturbations in a wide range of cell types and identified possible molecular mechanisms. We find that mediator complex subunit MED26 primarily regulates frequency, MYC regulates burst size, while cohesin and super-enhancers can modulate both. Despite comparable effect sizes on RNA levels amongst these perturbations, we find that acute depletion of MED26 plays a larger role in perturbing gene regulatory networks. Furthermore, this perturbation acts downstream of both chromatin spatial architecture and preinitiation complex formation, indicating that later steps in the initiation of transcriptional bursts are primary nodes for integrating gene networks in single cells.

2024-06-30 | GSE241338 | 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

Altered Cofactor Recruitment and Nucleosome Dynamics Underlie Bisphenol A's Impact on Estrogen Receptor-Mediated Transcriptional Bursting [ATAC-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 | GSE251650 | GEO

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

2025-06-02 | GSE251649 | GEO

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

2025-06-02 | GSE251651 | GEO

Transcriptional kinetics and molecular functions of long non-coding RNAs

Project description:An increasing number of long non-coding RNAs (lncRNAs) have confirmed important functions, yet little is known about their transcriptional dynamics and it remains challenging to determine their regulatory functions. Here, allele-sensitive single-cell RNA-seq was used to demonstrate that lncRNAs have lower burst frequencies compared to mRNAs. We observed an increased cell-to-cell variability in lncRNA expression that was due to more sporadic bursting (lower frequency) with larger numbers of RNA molecules being produced. Exploiting heterogeneity in asynchronously growing cells, we identified and experimentally validated lncRNAs with cell-state specific functions involved in cell cycle progression and apoptosis. Finally, we identified cis-functioning lncRNAs and knockdown of these lncRNAs modulated either transcriptional burst frequency or size of the nearby protein-coding gene. Collectively, we identify distinct transcriptional regulation of lncRNAs and we demonstrate a role for lncRNAs in the regulation of transcriptional bursting of mRNAs.

2021-11-19 | E-MTAB-11054 | biostudies-arrayexpress

Transcriptional Bursting and Co-bursting Regulation by Steroid Hormone Release Pattern and Transcription Factor Mobility

Project description:Transcriptional Bursting and Co-bursting Regulation by Steroid Hormone Release Pattern and Transcription Factor Mobility

| PRJNA548190 | ENA