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Transcription Pausing Regulates Mouse Embryonic Stem Cell Differentiation

ABSTRACT: Transcription Pausing Regulates Mouse Embryonic Stem Cell Differentiation

PROVIDER: PRJNA389555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5655560_1.fastq.gz	Fastqsanger.gz
	SRR5655560_2.fastq.gz	Fastqsanger.gz
	SRR5655670.fastq.gz	Fastqsanger.gz
	SRR5655671.fastq.gz	Fastqsanger.gz
	SRR5655672.fastq.gz	Fastqsanger.gz

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Transcription Pausing Regulates Mouse Embryonic Stem Cell Differentiation [GRO-seq]

Project description:The pluripotency of embryonic stem cells (ESCs) relies on appropriate responsiveness to developmental cues. Promoter-proximal pausing of RNA polymerase II (Pol II) has been suggested to play a role in keeping genes poised for future activation. To identify the role of Pol II pausing in regulating ESC pluripotency, we have generated mouse ESCs carrying a mutation in the pause-inducing factor SPT5. Consistent with previous in vitro studies showing the pausing deficiency of this mutant SPT5, our genomic analysis reveals genome-wide reduction of paused Pol II in mutant mESCs. Furthermore, we find that genes differentially regulated by mutant SPT5 correlates with distinct chromatin states. Functionally, this pausing-deficient SPT5 disrupts ESC differentiation without affecting self-renewal. Thus, our study uncovers an important role of Pol II pausing in regulating ESC differentiation and also suggests that Pol II pausing can both positively and negatively influence transcription depending on the local chromatin environment.

2017-12-08 | GSE99747 | GEO

Transcription Pausing Regulates Mouse Embryonic Stem Cell Differentiation [ATAC-seq]

2017-12-08 | GSE99746 | GEO

Transcription pausing regulates mouse embryonic stem cell differentiation.

Project description:The pluripotency of embryonic stem cells (ESCs) relies on appropriate responsiveness to developmental cues. Promoter-proximal pausing of RNA polymerase II (Pol II) has been suggested to play a role in keeping genes poised for future activation. To identify the role of Pol II pausing in regulating ESC pluripotency, we have generated mouse ESCs carrying a mutation in the pause-inducing factor SPT5. Genomic studies reveal genome-wide reduction of paused Pol II caused by mutant SPT5 and further identify a tight correlation between pausing-mediated transcription effect and local chromatin environment. Functionally, this pausing-deficient SPT5 disrupts ESC differentiation upon removal of self-renewal signals. Thus, our study uncovers an important role of Pol II pausing in regulating ESC differentiation and suggests a model that Pol II pausing coordinates with epigenetic modification to influence transcription during mESC differentiation.

| S-EPMC5732849 | biostudies-literature

Dynamic Change of Transcription Pausing through Modulating NELF Protein Stability Regulates Granulocytic Differentiation

Project description:The NELF complex is a metazoan-specific factor essential for establishing transcription pausing. Although NELF has been implicated in cell fate regulation, the cellular regulation of NELF and its intrinsic role in specific lineage differentiation remains largely unknown. Using mammalian hematopoietic differentiation as a model system, here we identified a dynamic change of NELF-mediated transcription pausing as a novel mechanism regulating hematopoietic differentiation. We found a sharp decrease of NELF protein abundance during granulocytic differentiation with a consequent genome-wide reduction of transcription pausing. This loss of pausing coincides with activation of granulocyte-affiliated genes and diminished expression of progenitor markers. Functional studies revealed that sustained expression of NELF inhibits granulocytic differentiation, whereas NELF depletion in progenitor cells leads to premature differentiation towards the granulocytic lineage. Our results thus uncover a previously unrecognized regulation of transcription pausing by modulating NELF protein abundance to control cellular differentiation.

2019-05-31 | GSE98555 | GEO

Transcription Factor p73 Regulates Th1 Differentiation

Project description:Transcription Factor p73 Regulates Th1 Differentiation

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Transcription Factor p73 Regulates Th1 Differentiation

Project description:Transcription Factor p73 Regulates Th1 Differentiation

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MED26-mediated phase separation regulates erythropoiesis by tuning transcription pausing

Project description:MED26-mediated phase separation regulates erythropoiesis by tuning transcription pausing

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MED26-mediated phase separation regulates erythropoiesis by tuning transcription pausing

Project description:The Mediator complex plays a pivotal role in various aspects of transcription and development. However, it remains unclear whether individual Mediator subunits play differential roles during the progression of the developmental process. In this study, we found that the protein level of MED26, a subunit in the core Mediator complex, remained relatively abundant in terminal erythropoiesis, while that of most Mediator subunits drastically diminished. MED26 exhibits pronounced phase separation capability, which is essential for erythroid differentiation of primary human erythroblasts. Interestingly, we found that ~60% of chromatin sites with MED26 or MED1 occupancy did not co-localize. Moreover, MED26-enriched loci were associated with RNA polymerase II pausing, and MED26 preferentially interacted with transcription pausing factors, including PAF1, via its TFIIS domain. During erythropoiesis, both the relative abundance of MED26 and the Pausing Index (PI) increased. Erythroid differentiation was promoted by small molecule-induced PI elevation or overexpression of MED26—full-length or the IDR alone—indicating that MED26-associated pausing is necessary for erythropoiesis. In conclusion, this study revealed that MED26 tunes transcription pausing to facilitate erythroid development via a phase separation mechanism.

2025-08-26 | GSE212374 | GEO

The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by pausing POL II at pro-differentiation genes [RNA-Seq]

Project description:In pluripotent cells, a delicate activation-repression balance maintains pro-differentiation genes ready for rapid transcription. The identity of transcription factors (TFs) that specifically repress pro-differentiation genes remains obscure. By targeting ~1,700 TFs with CRISPR loss-of-function perturbations, we found that ZBTB11 and ZFP131 are required to maintain pluripotency in mouse embryonic stem cells (ESCs). ZBTB11 and ZFP131 bind to pro-differentiation genes along with RNA Polymerase II and pausing factor NELF, but without Polycomb repression. Loss of ZBTB11 or ZFP131 leads to a decrease in NELF binding, an increase in H3K4me3, transcriptional upregulation of genes associated with three germ layers, and concomitant ESC differentiation. Together, our results suggest ZBTB11 and ZFP131 maintain pluripotency by pausing pro-differentiation genes transcription and present a generalizable framework to maintain cellular potency.

2022-01-07 | GSE160960 | GEO

The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by pausing POL II at pro-differentiation genes [sgRNA-seq]

2022-01-07 | GSE160963 | GEO