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Mus musculus

ABSTRACT: CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [HiC-Seq]

PROVIDER: PRJNA353555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5016460_1.fastq.gz	Fastqsanger.gz
	SRR5016460_2.fastq.gz	Fastqsanger.gz
	SRR5016461_1.fastq.gz	Fastqsanger.gz
	SRR5016461_2.fastq.gz	Fastqsanger.gz
	SRR5016462_1.fastq.gz	Fastqsanger.gz

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CTCF translates IL-2- and aKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs

Project description:CTCF translates IL-2- and aKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs

| PRJNA353354 | ENA

Mus musculus

Project description:CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [ATAC-Seq]

| PRJNA353554 | ENA

Mus musculus

Project description:CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [ChIP-Seq]

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Mus musculus

Project description:CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [RNA-Seq]

| PRJNA353552 | ENA

CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [HiC-Seq]

Project description:We found that aspects of the IL-2-sensitive effector gene program in CD4+ Th1 and CD8+ Tc1 cells are regulated by glutamine and alpha-ketoglutarate (αKG)-induced events, in part through changes in DNA and histone methylation states. We further identified a novel mechanism by which IL-2- and αKG-sensitive metabolic changes regulate the association of CTCF with select genomic sites. αKG-sensitive CTCF sites were often associated with loci containing IL-2- and αKG-sensitive genome organization patterns and gene expression in T cells. Surprisingly, IL-2- and αKG-sensitive CTCF sites in T cells were also associated with genes from developmental pathways that had αKG-sensitive expression in ES cells. The data collectively support a novel mechanism wherein CTCF serves to translate αKG-sensitive metabolic changes into context-dependent differentiation gene programs.

2017-08-15 | GSE89676 | GEO

CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [ATAC-Seq]

2017-08-15 | GSE89038 | GEO

CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [ChIP-Seq]

2017-08-15 | GSE88857 | GEO

CTCF translates IL-2- and αKG-sensitive metabolic changes in T cells into context-dependent differentiation gene programs [RNA-Seq]

2017-08-15 | GSE88829 | GEO

Nucleosome repositioning links DNA (de)methylation and differential CTCF binding during stem cell development

Project description:During differentiation of embryonic stem cells, chromatin reorganizes to establish cell type specific expression programs. Here, we have dissected the linkages between DNA methylation (5mC), hydroxymethylation (5hmC), nucleosome repositioning and binding of the transcription factor CTCF during this process. By integrating MNase-seq and ChIP-seq experiments in mouse embryonic stem cells (ESC) and their differentiated counterparts with biophysical modeling, we find that the interplay between these factors depends on their large-scale genomic context. The mostly unmethylated CpG islands have a reduced nucleosome occupancy and are enriched in cell type-independent binding sites for CTCF. The few remaining methylated CpG dinucleotides are preferentially associated with nucleosomes. In contrast, outside of CpG islands most CpGs are methylated and their average density oscillates so that it is highest in the linker region between nucleosomes. Outside CpG islands binding of TET1, an enzyme that converts 5mC to 5hmC, is associated with labile, MNase-sensitive nucleosomes. Such nucleosomes are poised for eviction in ESCs and become stably bound in differentiated cells where the level of TET1 and 5hmCs goes down. In particular, this has a dramatic effect at variable CTCF sites enriched outside CpG islands, that are occupied by CTCF in ESCs but loose CTCF during differentiation. To rationalize this cell type dependent targeting of CTCF binding in competition with the histone octamer, we have developed a quantitative biophysical model, which allowed predicting differences in CTCF binding due to TET1/5hmC/5mC-dependent nucleosome repositioning.

2014-05-07 | GSE56938 | GEO

Metabolic regulation of CTCF expression and chromatin association dictates starvation response in mice and flies

Project description:Temporal and coordinated control of gene expression is vital to mount appropriate physiological responses, especially in the context of dynamic metabolic transitions. Despite this, the interplay between chromatin architectural proteins and metabolism in regulating transcription is largely unknown. Here, we demonstrate that CTCF, the transcriptional regulator and boundary insulating protein, is itself regulated by metabolic inputs and its expression is associated with fed/fasted states. Although CTCF is well established as a key determinant of gene expression programs, our results indicate that its loci-specific functional diversity is associated with physiological plasticity during fed-fast cycles. Intriguingly, CTCF ChIP-seq and its differential expression point towards a paradoxical and yet tuneable binding to chromatin, as a function of hepatic metabolic status. Given emerging literature that indicates loci-/affinity-dependent functions of CTCF, we illustrate a physiological setting for such disparate association that is possibly mediated by the abundance of a non-coding RNA, Jpx. Further, meta-analyses of fed-fast dependent global transcriptional response and CTCF occupancy hint at the crucial role of CTCF in dictating hepatic gene expression and metabolism. Importantly, altering CTCF expression influenced the temporal cascade of metabolic gene expression. Heterologous perturbation of CTCF, to levels that mimic physiological oscillation, impacted mitochondrial energetics and lipidome profiles in hepatocytes. In addition to demonstrating the significance of CTCF expression and its differential chromatin association, our study also highlights the interplay between metabolism and chromatin organizers.

2023-07-04 | GSE207692 | GEO

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