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Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [RNA-seq]

ABSTRACT: Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [RNA-seq]

PROVIDER: PRJNA434730 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6754310.fastq.gz	Fastqsanger.gz
	SRR6754320.fastq.gz	Fastqsanger.gz
	SRR6754330.fastq.gz	Fastqsanger.gz
	SRR6754311.fastq.gz	Fastqsanger.gz
	SRR6754321.fastq.gz	Fastqsanger.gz

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Similar Datasets

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

Project description:Multipotent progenitors confirm their T-lineage identity at the DN2a to DN2b pro-T cell transition, when expression of the essential transcription factor Bcl11b begins. This study defines the molecular basis of direct and indirect actions of Bcl11b in acquisition of T cell identity. In vivo and in vitro stage-specific deletions identify functional regulation targets genome-wide for mechanistic analysis. Bcl11b can associate with multiple co-factors and its direct action is needed to recruit these to selective target sites. Sites of Bcl11b-dependent cofactor recruitment are enriched at functionally regulated targets, and deletion of individual cofactors can relieve repression of many Bcl11b-repressed genes. In parallel, Bcl11b indirectly regulates a subset of its target genes by a gene network circuit via Id2 and Zbtb16, which are directly repressed by Bcl11b and control distinct alternative programs.

2018-09-21 | GSE110305 | GEO

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [RNA-seq]

2018-09-21 | GSE110882 | GEO

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [ChIP-seq]

2018-09-21 | GSE115742 | GEO

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

| PRJNA433410 | ENA

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16

| PRJNA475900 | ENA

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [ChIP-seq]

Project description:Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16 [ChIP-seq]

| PRJNA475905 | ENA

Bcl11b sets pro-T cell fate by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.

Project description:Multipotent progenitor cells confirm their T cell-lineage identity in the CD4-CD8- double-negative (DN) pro-T cell DN2 stages, when expression of the essential transcription factor Bcl11b begins. In vivo and in vitro stage-specific deletions globally identified Bcl11b-controlled target genes in pro-T cells. Proteomics analysis revealed that Bcl11b associated with multiple cofactors and that its direct action was needed to recruit those cofactors to selective target sites. Regions near functionally regulated target genes showed enrichment for those sites of Bcl11b-dependent recruitment of cofactors, and deletion of individual cofactors relieved the repression of many genes normally repressed by Bcl11b. Runx1 collaborated with Bcl11b most frequently for both activation and repression. In parallel, Bcl11b indirectly regulated a subset of target genes by a gene network circuit via the transcription inhibitor Id2 (encoded by Id2) and transcription factor PLZF (encoded by Zbtb16); Id2 and Zbtb16 were directly repressed by Bcl11b, and Id2 and PLZF controlled distinct alternative programs. Thus, our study defines the molecular basis of direct and indirect Bcl11b actions that promote T cell identity and block alternative potentials.

| S-EPMC6240390 | biostudies-literature

Bcl11b defines pro-T identity by site-specific cofactor recruitment and by repressing Id2 and Zbtb16

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

2018-09-21 | GSE115744 | GEO

Transcriptome analysis of Bcl11b-deficient murine NK cells

Project description:Epigenetic landscapes can provide insight into regulation of gene expression and cellular diversity. Here, we examined the transcriptional and epigenetic profiles of seven human blood NK cell populations, including adaptive NK cells. The BCL11B gene, encoding a transcription factor (TF) essential for T cell development and function, was the most extensively regulated, with expression increasing throughout NK cell differentiation. Several Bcl11b-regulated genes associated with T cell-signaling were specifically expressed in adaptive NK cell subsets. Regulatory networks revealed reciprocal regulation at distinct stages of NK cell differentiation, with Bcl11b repressing RUNX2 and ZBTB16 in canonical and adaptive NK cells, respectively. A critical role for Bcl11b in driving NK cell differentiation was corroborated in BCL11B mutated patients and by ectopic Bcl11b expression. Moreover, Bcl11b was required for adaptive NK cell responses in a murine CMV model, supporting expansion of these cells. Together, we define the TF regulatory circuitry of human NK cells and uncover a critical role for Bcl11b in promoting NK cell differentiation and function.

2021-05-28 | GSE162472 | GEO

Cell-type specific action of Bcl11b in early T-lineage and group 2 innate lymphoid cell

Project description:The zinc finger transcription factor, Bcl11b, is expressed in T cells and group 2 innate lymphoid cells (ILC2s) among hematopoietic cells. In early T-lineage cells, Bcl11b directly binds and represses endogenous E protein antagonist, Id2, expression to prevent pro-T cell from adopting an innate-like fate. In contrast, ILC2s co-express both Bcl11b and Id2. Here, to address this contradiction, we have directly compared Bcl11b action mechanisms in pro-T cells and ILC2s. We found that Bcl11b binds to distinctive genomic regions across the genome with cell-type specific motif preferences. Bcl11b occupies functionally different sites in lineage specific way and controls totally different sets of target genes, while both of cell types use the same distal enhancer region to control timing of Bcl11b activation. In addition, Bcl11b seems to have cell-type specific post-translational modifications and to organize differential protein complexes. Therefore, despite pro-T cells and ILC2s share Bcl11b for their optimal development and function, Bcl11b is able to regulate substantially different target genes.

2019-10-19 | GSE131082 | GEO

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