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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [ChIP-seq]

ABSTRACT: Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [ChIP-seq]

PROVIDER: PRJNA1130975 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29684761.fastq.gz	Fastqsanger.gz
	SRR29684762.fastq.gz	Fastqsanger.gz
	SRR29684763.fastq.gz	Fastqsanger.gz
	SRR29684764.fastq.gz	Fastqsanger.gz
	SRR29684765.fastq.gz	Fastqsanger.gz

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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNA-Seq]

Project description:We previously demonstrated that the NF-κB inhibitor IκBα binds the chromatin together with PRC2 to regulate a subset of developmental- and stem cell-related genes. This alternative function has been elusive in both physiological and disease conditions because of the predominant role of IκBα as a negative regulator of NF-κB. We here uniquely characterize specific residues of IκBα that allow the generation of separation-of-function (SOF) mutants that are defective for either NF-κBrelated (SOF DeltaNF-κB) or chromatin-related (SOF DeltaH2A,H4) activities. Expression of IκBα SOF DeltaNF-κB, but not SOF DeltaH2A/H4, is sufficient to negatively regulate a specific stemness program in intestinal cells, thus rescuing the differentiation blockage imposed by IκBα deficiency. . By ChIP assay we demonstrated IκBα binding to several stem cell genes that are transcriptionally repressed following IκBα SOF DeltaNF-κB induction. Our data indicate that SOF mutants represent an exclusive tool for studying IκBα functions in physiology and disease.

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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [ChIP-seq]

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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNAseq Knock-ins IKBa]

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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness

Project description:Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness

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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNA-Seq]

Project description:Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNA-Seq]

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Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNAseq Knock-ins IKBa]

Project description:Separation-of-function mutants reveal the NF-κB-independent involvement of IκBα in the regulation of intestinal stemness [RNAseq Knock-ins IKBa]

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Chromatin activity of IκBα mediates the exit from naïve pluripotency (RNA-Seq)

Project description:Inflammatory signals are key in development and cell differentiation but their orchestration with pluripotency and stemness signals is poorly understood. Our previous work identified a chromatin function of IκBα, the NF-κB inhibitor, that is crucial for differentiation in different types of somatic stem cells. Here we demonstrate that deficiency of IκBα imposes a profound chromatin rewiring defect that impacts on DNA methylation, histone post-translational modifications and transcriptional regulation, stabilizing mouse embryonic stem cells (ESCs) in a ground state of pluripotency while preventing them from pluripotency exit and differentiation. By engineering separation-of-function mutants of IκBα with specific binding to either NF-κB or histones, we demonstrate that regulation of pluripotency state by IκBα is independent of NF-kB but requires the chromatin-related IκBα function.

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Chromatin activity of IκBα mediates the exit from naïve pluripotency (Methylation array)

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Chromatin activity of IκBα mediates the exit from naïve pluripotency (ChIP-seq Histone marks)

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Expression data from RH30 vector and RH30 IκBα SR cells

Project description:Classical NF-κB activity can be inhibited by overexpression of the IκBα super repressor (SR). To determine the role of NF-κB in rhabdomyosarcoma cells, we overexpressed the IκBα SR in RH30 rhabdomyosarcoma cells. IκBα SR was overexpressed in RH30 cells. RH30 vector cells were used as control group.

2018-03-30 | GSE112119 | GEO

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