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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE115744 | GEO | 2018/09/21

REPOSITORIES: GEO

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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 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 [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

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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]

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

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

| PRJNA434730 | ENA

Ovol1 regulates meiotic pachytene progression during spermatogenesis by repressing Id2 expression.

Project description:Previous studies have shown that a targeted deletion of Ovol1 (previously known as movo1), encoding a member of the Ovo family of zinc-finger transcription factors, leads to germ cell degeneration and defective sperm production in adult mice. To explore the cellular and molecular mechanism of Ovol1 function, we have examined the mutant testis phenotype during the first wave of spermatogenesis in juvenile mice. Consistent with the detection of Ovol1 transcripts in pachytene spermatocytes of the meiotic prophase, Ovol1-deficient germ cells were defective in progressing through the pachytene stage. The pachytene arrest was accompanied by an inefficient exit from proliferation, increased apoptosis and an abnormal nuclear localization of the G2-M cell cycle regulator cyclin B1, but was not associated with apparent chromosomal or recombination defects. Transcriptional profiling and northern blot analysis revealed reduced expression of pachytene markers in the mutant, providing molecular evidence that pachytene differentiation was defective. In addition, the expression of Id2 (inhibitor of differentiation 2), a known regulator of spermatogenesis, was upregulated in Ovol1-deficient pachytene spermatocytes and repressed by Ovol1 in reporter assays. Taken together, our studies demonstrate a role for Ovol1 in regulating pachytene progression of male germ cells, and identify Id2 as a Ovol1 target.

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Cdc42 defines apical identity and regulates epithelial morphogenesis by promoting apical recruitment of Par6-aPKC and Crumbs.

Project description:Cdc42 regulates epithelial morphogenesis together with the Par complex (Baz/Par3-Par6-aPKC), Crumbs (Crb/CRB3) and Stardust (Sdt/PALS1). However, how these proteins work together and interact during epithelial morphogenesis is not well understood. To address this issue, we used the genetically amenable Drosophila pupal photoreceptor and follicular epithelium. We show that during epithelial morphogenesis active Cdc42 accumulates at the developing apical membrane and cell-cell contacts, independently of the Par complex and Crb. However, membrane localization of Baz, Par6-aPKC and Crb all depend on Cdc42. We find that although binding of Cdc42 to Par6 is not essential for the recruitment of Par6 and aPKC to the membrane, it is required for their apical localization and accumulation, which we find also depends on Par6 retention by Crb. In the pupal photoreceptor, membrane recruitment of Par6-aPKC also depends on Baz. Our work shows that Cdc42 is required for this recruitment and suggests that this factor promotes the handover of Par6-aPKC from Baz onto Crb. Altogether, we propose that Cdc42 drives morphogenesis by conferring apical identity, Par-complex assembly and apical accumulation of Crb.

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