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Mus musculus

ABSTRACT: Genome-wide maps of Egr2 transcription factor binding sites in NKT and anti TCRb injected thymocytes.

PROVIDER: PRJNA149755 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR388185.fastq.gz	Fastqsanger.gz
	SRR388186.fastq.gz	Fastqsanger.gz
	SRR388187.fastq.gz	Fastqsanger.gz
	SRR388188.fastq.gz	Fastqsanger.gz
	SRR388189.fastq.gz	Fastqsanger.gz

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Genome-wide maps of Egr2 transcription factor binding sites in NKT and anti TCRb injected thymocytes.

Project description:We report the application of single-molecule-based sequencing technology for mapping the Egr2 transcriptional program in developing thymic NKT. We found that Egr2 controls the induction of genes required for NKT development. Examination of developing NKT cells and thymocytes receiving a strong TCR signal in vivo by injecting 500ug anti-TCRb antibody.

2012-02-06 | E-GEOD-34254 | biostudies-arrayexpress

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Project description:Genome-wide maps of EGR2 transcription factor binding sites in T cell anergy

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Genome-wide maps of EGR2 transcription factor binding sites in T cell anergy

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Genome-wide maps of Egr2 transcription factor binding sites in NKT and anti TCRb injected thymocytes.

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NKT-10 cells represent a novel invariant NKT cell subset with regulatory characteristics

Project description:We compared splenic Va14i NKT cells from C57BL/6 control mice and from mice injected 4 weeks earlier intravenously with 4ug/mouse of the iNKT cell antigen alpha-galactosylceramide (aGalCer). These mice were either left unstimulated or were stimulated with 1ug/mouse aGalCer i.v.. All mice were female and 8 weeks of age at the beginning of the experiment. Va14i NKT cells were enriched via magnetic selection and cell sorted for TCRb+ CD1d/aGalCer-tetramer+. Total RNA were prepared using a Qiagen RNeasy mini kit. IVT probe generation and hybridization to Affymetrix Mouse Genome 430 2.0 arrays was carried out by the Veterans Medical Research Foundation GeneChipTM Microarray located at UCSD. Group 1 (Ctr_unstim) = iNKT cells from C57BL/6 control mice and left unstimulated / Group 2 (Ctr_stim) = iNKT cells from C57BL/6 control mice and injected 1h before purification with 1ug aGalCer i.v. / Group 3 (Pre_unstim) = iNKT cells from C57BL/6 mice injected 4weeks earlier with 4ug aGalCer i.v. and left unstimulated / Group 4 (Pre_stim) = iNKT cells from C57BL/6 mice injected 4weeks earlier with 4ug aGalCer i.v. and injected 1h before purification with 1ug aGalCer i.v. / Sample were prepared in duplicates in two independent experiments.

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GFP-Egr2 ChIP-seq analysis of CD4 T cells

Project description:Identification of Egr2 binding sites in CD4 T cells from GFP-Egr2 knockin (Egr2 Kin) mice by GFP-Egr2 ChIP-seq

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Project description:Natural killer T (NKT) cells identified by CD1d-tetramer and TCRb were isolated from the thymi of wild type and Ezh2 knockout mice. The NKT cells were FACS sorted into different stages based on the surface expression of CD44 and NK1.1.

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Multiple levels of transcriptional regulation by PLZF in NKT cell development [human_ChIP-seq]

Project description:Using biotinylation-based ChIP-seq and microarray analysis of both NKT and PLZF-transgenic thymocytes, we identified several layers of regulation of the innate-like NKT effector program. The transcription factor PLZF is induced during the development of innate and innate-like lymphocytes to direct their acquisition of a T helper effector program, but the molecular mechanisms involved are poorly understood. Using biotinylation-based ChIP-seq and microarray analysis of both NKT and PLZF-transgenic thymocytes, we identified several layers of regulation of the innate-like NKT effector program: first, PLZF bound and regulated genes encoding cytokine receptors as well as homing and adhesion receptors; second, PLZF bound and activated T helper-specific transcription factor genes that in turn control T helper specific programs; finally, PLZF bound and suppressed the transcription of Bach2, a potent general repressor of effector differentiation in naive T cells. These findings reveal the architecture of the transcriptional program recruited by PLZF and elucidate how a single transcription factor can drive the developmental acquisition of a broad effector program.

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