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

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

PROVIDER: PRJNA675001 | ENA |

REPOSITORIES: ENA

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The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by pausing POL II at pro-differentiation genes [sgRNA-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 | GSE160963 | GEO

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

2022-01-07 | GSE160962 | GEO

The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by pausing POL II at pro-differentiation genes [ChIP-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 association, 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 | GSE160959 | GEO

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

2022-01-07 | GSE160960 | GEO

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

Project description:The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by pausing POL II at pro-differentiation genes

| PRJNA675007 | ENA

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

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

| PRJNA675002 | ENA

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

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

| PRJNA675004 | ENA

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

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

| PRJNA675005 | ENA

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

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

2022-01-07 | GSE160966 | GEO

Spatial transcriptomics unveils ZBTB11 as a regulator of cardiomyocyte degeneration in cardiomyopathy

Project description:Aims Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac disorder that is characterized by progressive fibro-fatty replacement of the myocardium, arrhythmias, and sudden death. While myocardial degeneration and fibro-fatty replacement occurs in specific locations, the underlying molecular changes remain poorly characterized. Here we aim to delineate local changes in gene expression to help identify new genes or pathways that are relevant for specific remodelling processes occurring during ACM. Methods and Results Using Tomo-Seq, a genome-wide transcriptional profiling with high spatial resolution, we created a transmural epicardial to endocardial gene expression atlas of an explanted ACM heart to gain molecular insights into disease-driving processes. This enabled us to link gene expression profiles to the different regional remodelling responses and allowed us to identify genes that are potentially relevant for disease progression. In doing we revealed BTB (broad-complex, tramtrack, bric-à-brac) domain containing 11 (ZBTB11) to be specifically enriched at sites of active fibrofatty replacement of myocardium. Immunohistochemistry indicated ZBTB11 to be enriched in cardiomyocytes flanking fibrofatty areas, which could be confirmed in multiple cardiomyopathy patients. Forced overexpression of ZBTB11 in iPS-derived cardiomyocytes showed ZBTB11 to function as a potent inducer of cardiomyocyte atrophy. Conclusion By combining spatial transcriptomics with classical histological approaches we identified gene expression changes underlying local remodelling responses in ACM. In doing so we found ZBTB11 to function as a relevant driver of cardiomyocyte atrophy. These data show the power of Tomo-Seq to unveil new molecular mechanisms and indicate ZBTB11 as a potential new target for cardiomyopathy.

2021-05-22 | GSE114770 | GEO

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