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DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (Dnase-Seq)

ABSTRACT: DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (Dnase-Seq)

PROVIDER: PRJNA598169 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10804500_1.fastq.gz	Fastqsanger.gz
	SRR10804500_2.fastq.gz	Fastqsanger.gz
	SRR10804501_1.fastq.gz	Fastqsanger.gz
	SRR10804501_2.fastq.gz	Fastqsanger.gz
	SRR10804502_1.fastq.gz	Fastqsanger.gz

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DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (Dnase-Seq)

Project description:Using the Notch signaling pathway, hematopoietic stem and progenitor cells (HSPC) sense and respond to the surrounding microenvironment to regulate cell fate outcome. Our previous studies have indicated that quantitative differences in Notch signal strength mediate cell-fate decisions during hematopoiesis. Low signal strength favors HSPC self-renewal, along with inhibition of myelopoiesis, whereas high signal strength promotes T cell differentiation. The basis for target gene selectivity in response to quantitative differences in Notch signal strength is unknown. Focusing on the high dose dependent induction of the T cell lineage, we found that targets essential for T cell commitment, including IL2ra, CD3 and Rag1, establish promoter DNA accessibility only upon exposure to high levels of Notch signaling. We further find that low promoter CpG content is a feature capable of maintaining the ground state DNA inaccessibility of these lineage determining genes. Our results suggest that DNA inaccessibility at the promoters of essential T cell commitment genes, mediated in part through low CpG content, provides robust protection against stochastic activation in inappropriate Notch signaling contexts, ensuring the maintenance of HSPC developmental plasticity.

2021-03-25 | GSE142736 | GEO

DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (RNA-Seq)

2021-03-25 | GSE142738 | GEO

DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression

Project description:DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression

| PRJNA598166 | ENA

DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (RNA-Seq)

Project description:DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression (RNA-Seq)

| PRJNA598171 | ENA

Single-Cell RNA Sequencing of Thymic KN6 γδ T-Cells Modulated by TCR Signal Strength and Notch Signaling

Project description:γδ T-cells form an integral arm of the immune system through their rapid and potent effector functions, and are critical players during both protective and destructive immunity. However, the factors that dictate γδ T-cell functional programming in vivo remain to be fully elucidated. Here, we employed RBPJ-inducible and KN6-transgenic mice to assess the roles of ontogenic timing, T-cell receptor (TCR) signal strength, and Notch signaling in the generation of γδ T-cell functional subsets in vivo. We found skewed generation of Vγ1+ cells toward the PLZF+ γδ T-cell lineage at the fetal stage. Similarly, generation of interleukin (IL)-17 producing γδ T-cells was favored during, although not exclusive to, the fetal stage. Strong TCR signals, in conjunction with Notch, were necessary for the generation of IL-4 producing γδ T-cells. Conversely, weak TCR signals were amenable for the generation of IL-17 producing γδ T-cells, which was Notch-independent. Additionally and surprisingly, Notch signaling was also dispensable for peripheral γδ T-cell IL-17 production. Thus, our results precisely defined the roles of ontogenic timing, TCR signal strength, and Notch signaling in γδ T-cell functional programming in vivo.

2021-05-01 | GSE165908 | GEO

DNA accessibility determines the level of Notch signal strength necessary for lineage specific target gene expression

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

2021-03-25 | GSE142739 | GEO

T cell receptor signal strength and antigen affinity differentially regulate memory CD8+ T cell development

Project description:IL-2 inducible tyrosine kinase (Itk) is a Tec family non-receptor tyrosine kinase that is known to regulate T cell receptor signal strength (TcR) and T cell development and differentiation. TcR signal strength and antigen affinity are parameters known to regulate the development of CD8+ T cell memory. However, the intersection between TcR signal strength and antigen affinity on CD8+ memory T cell development remains unclear. Therefore, we compared the transcriptomes of WT and Itk-/- OT-1/Rag-/- CD8+ T cells at day 0 and day 7 following infection with Listeria monocytogenes expressing the SIINFEKL (N4) or SIITFEKL (T4) OVA peptide variant (different affinities for TcR) by RNA sequencing.

2020-09-30 | GSE137406 | GEO

TCR signal strength controls thymic differentiation of iNKT cell subsets

Project description:TCR signal strength controls thymic differentiation of iNKT cell subsets

| PRJNA433481 | ENA

TCR signal strength controls thymic differentiation of iNKT cell subsets

Project description:TCR signal strength controls thymic differentiation of iNKT cell subsets

| PRJNA436981 | ENA

TCR signal strength controls thymic differentiation of iNKT cell subsets

Project description:Three major phenotypically and functionally distinct invariant Natural Killer T (iNKT) cell subsets (iNKT1, iNKT17 and iNKT2), each with propensity to traffic to different tissues and to secrete different cytokines upon activation, have been defined. These fate assignments can be conferred upon iNKT cells during development in the thymus, but the cues that direct these decisions remain unclear. Here, we show that T cell antigen receptor (TCR) signal strength governs the development of iNKT cell subsets in the thymus, with high signaling strength necessary for iNKT2 and iNKT17 development. Alteration of TCR diversity and/or signaling dramatically diminished iNKT2 and iNKT17 cell subset development in a cell intrinsic manner. Decreased TCR signaling affected the persistence of Egr2 expression and the upregulation of PLZF both in vivo and in vitro. Genome-wide chromatin accessibility analysis revealed subset-specific activity of regulatory elements associated with unique signatures of transcription factor binding sites. NFAT and Egr binding motifs were found preferentially enriched in chromatin regulatory regions specifically accessible in iNKT2 cells that were lost in iNKT2 cells that had developed with reduced TCR signaling. Altogether, these data suggest a model of iNKT cell subset development where variable TCR signaling induces changes in chromatin accessibility at NFAT and Egr binding sites which exerts a determinative influence on the dynamic of gene enhancer accessibility that affects the developmental fate of iNKT cells.

2018-05-18 | GSE111427 | GEO

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