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A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus.

ABSTRACT: A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus.

PROVIDER: PRJNA480688 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7289430.fastq.gz	Fastqsanger.gz
	SRR7289440.fastq.gz	Fastqsanger.gz
	SRR7289450.fastq.gz	Fastqsanger.gz
	SRR7289431.fastq.gz	Fastqsanger.gz
	SRR7289441.fastq.gz	Fastqsanger.gz

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A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus [DamID]

Project description:Tcrb locus V(D)J recombination is regulated by positioning at the nuclear periphery. Here we used DamID to profile Tcrb locus interactions with the nuclear lamina at high-resolution. We identified a lamina-associated domain (LAD) border composed of several CTCF binding elements that segregates active non-LAD from inactive LAD regions of the locus. Deletion of the LAD border caused an enhancer-dependent spread of H3K27ac from the active recombination center into recombination center-proximal LAD chromatin. This was associated with a disruption to LAD organization, increased chromatin looping to the recombination center, and increased transcription and recombination of recombination center-proximal gene segments. Our results show that a Tcrb locus LAD and LAD border are critical components of Tcrb locus gene regulation and suggest that LAD borders may generally function to constrain the activity of nearby enhancers.

2018-10-22 | GSE116953 | GEO

A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus [ChIP-seq]

2018-10-22 | GSE115582 | GEO

A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus [DamID]

Project description:A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus [DamID]

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A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus [ChIP-seq]

Project description:A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus [ChIP-seq]

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A Lamina-Associated Domain Border Governs Nuclear Lamina Interactions, Transcription, and Recombination of the Tcrb Locus.

Project description:Tcrb locus V(D)J recombination is regulated by positioning at the nuclear periphery. Here, we used DamID to profile Tcrb locus interactions with the nuclear lamina at high resolution. We identified a lamina-associated domain (LAD) border composed of several CTCF-binding elements that segregates active non-LAD from inactive LAD regions of the locus. Deletion of the LAD border causes an enhancer-dependent spread of histone H3 lysine 27 acetylation from the active recombination center into recombination center-proximal LAD chromatin. This is associated with a disruption to nuclear lamina association, increased chromatin looping to the recombination center, and increased transcription and recombination of recombination center-proximal gene segments. Our results show that a LAD and LAD border are critical components of Tcrb locus gene regulation and suggest that LAD borders may generally function to constrain the activity of nearby enhancers.

| S-EPMC6287930 | biostudies-literature

A lamina-associated domain border governs nuclear lamina interactions, transcription and recombination of the Tcrb locus.

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

2018-10-22 | GSE116954 | GEO

Regulatory T cells from colonic lamina propria [array]

Project description:The colonic lamina propria contains a distinct population of Foxp3+ T regulatory cells (Tregs) that modulate responses to commensal microbes. Analysis of gene expression revealed that the transcriptome of colonic Tregs is distinct from splenic and other tissue Tregs. Rorγ and Helios in colonic Tregs mark distinct populations: Rorγ+Helios- or Rorγ-Helios+ Tregs. We uncovered an unanticipated role for Rorγ, a transcription factor generally considered to be antagonistic to Foxp3. Rorγ in colonic Tregs accounts for a small but specific part of the colon-specific Treg signature. (1) Total colonic and splenic Foxp3+ Treg comparison: Lymphocytes were isolated from colonic lamina propria and spleens of Foxp3-ires-GFP mice, where GFP reports Foxp3 expression. TCRb+CD4+GFP+ cells were double sorted into Trizol. (2) Colonic Rorγ+ and Rorγ- Treg comparison: Foxp3-ires-Thy1.1 reporter mice were crossed to Rorc-GFP reporter mice to generate mice that report both Foxp3 and Rorγ expression. Rorγ+Foxp3+ Tregs (TCRb+CD4+Thy1.1+GFP+) and Rorγ-Foxp3+ Tregs (TCRb+CD4+Thy1.1+GFP-) from colonic lamina propria were double sorted into Trizol.To reduce variability and increase cell number, cells from multiple mice were pooled for sorting and at least three replicates were generated for all groups. RNA from 1.5-3.0 x104 cells was amplified, labeled and hybridized to Affymetrix Mouse Gene 1.0 ST Arrays.

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16S-seq analysis of the microbiota of WT and TCRb-/- mice

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Tissue-specific changes in Tcrb conformation

Project description:We report the changes in Tcrb interactome upon transitioning from DN to DP stage of thymocyte development

2015-07-08 | GSE68955 | GEO

Peripheral subnuclear positioning suppresses Tcrb recombination and segregates Tcrb alleles from RAG2.

Project description:Allelic exclusion requires that the two alleles at antigen-receptor loci attempt to recombine variable (V), diversity (D), and joining (J) gene segments [V(D)J recombination] asynchronously in nuclei of developing lymphocytes. It previously was shown that T-cell receptor ? (Tcrb) alleles frequently and stochastically associate with the nuclear lamina and pericentromeric heterochromatin in CD4(-)CD8(-) thymocytes. Moreover, rearranged alleles were underrepresented at these locations. Here we used 3D immunofluorescence in situ hybridization to identify recently rearranged Tcrb alleles based on the accumulation of the DNA-repair protein 53BP1. We found that Tcrb alleles recombine asynchronously in double-negative thymocytes and that V(D)J recombination is suppressed on peripheral as compared with central Tcrb alleles. Moreover, the recombination events that did take place at the nuclear periphery preferentially occurred on Tcrb alleles that were partially dissociated from the nuclear lamina. To understand better the mechanism by which V(D)J recombination is suppressed at the nuclear periphery, we evaluated the subnuclear distribution of recombination-activating gene 2 (RAG2) protein. We found that RAG2 abundance was reduced at the nuclear periphery. Moreover, RAG2 was distributed differently from RNA polymerase II and histone H3K4 trimethylation. Our data suggest that the nuclear periphery suppresses V(D)J recombination, at least in part, by segregating Tcrb alleles from RAG proteins.

| S-EPMC3845165 | biostudies-literature

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