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A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction

ABSTRACT: A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction

PROVIDER: PRJNA517696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8487420_1.fastq.gz	Fastqsanger.gz
	SRR8487420_2.fastq.gz	Fastqsanger.gz
	SRR8487421_1.fastq.gz	Fastqsanger.gz
	SRR8487421_2.fastq.gz	Fastqsanger.gz
	SRR8487413_1.fastq.gz	Fastqsanger.gz

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A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction [Capture-C]

Project description:Loss of function of CDKN2A/B, also known as INK4/ARF [encoding for p16INK4A, p15INK4B, and p14ARF (mouse p19Arf)]), confers susceptibility to cancers, whereas its up-regulation during organismal aging provokes cellular senescence and tissue degenerative disorders. To better understand molecular regulation of the locus, we knocked P2A-mCherry into the C-terminus of p16INK4A, and this construct faithfully recapitulated the endogenous transcription. Using this reporter cell line, we performed a noncoding tiling pooled screening targeting open chromatin regions spanning the approximately 500-kb region in the topological associated domain that includes p16INK4A. In both Cas9- and dCas9-KRAB–mediated screenings, we identified a 42-bp DNA sequence within exon 1β of the ARF gene, as the repressive element controlling p16INK4A expression. Chromatin conformation capture indicated that inactivating this element abolished the physical interaction between p15INK4B and ARF, thereby abolishing p16INK4A repression. This study has revealed a new mechanism of transcriptional regulation of p16INK4A by long-range chromatin interaction.

2019-12-17 | GSE125666 | GEO

A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction [Cut&Run ChiP-seq]

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A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction [Capture-C]

Project description:A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction [Capture-C]

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A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction [Cut&Run ChiP-seq]

Project description:A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction [Cut&Run ChiP-seq]

| PRJNA517697 | ENA

A minimal DNA sequence within the ARF promoter represses p16INK4A expression via long-range chromatin interaction

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

2019-12-17 | GSE125842 | GEO

Expression data from Bmi1-overexpressing Ink4a-Arf-null hepatoblasts

Project description:Forced expression of Bmi1 accelerated the self-renewal of hepatic stem/progenitor cells and eventually induced their transformation in an in vivo transplant model. The Ink4a/Arf locus, which encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf, is a pivotal target of Bmi1. Therefore, it would be of importance to understand the contribution of the Ink4a/Arf locus to Bmi1 oncogenic functions in cancer and search for as-yet-unknown Bmi1 target genes other than Ink4a/Arf. We used microarrays to explore novel candidate downstream targets for Bmi1 in hepatic stem/progenitor cells

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The transcription Factor Slug represses p16Ink4a and regulates murine muscle stem cell aging

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Cysteine oxidation triggers amyloid fibril formation of the tumor suppressor p16INK4A

Project description:p16INK4A inhibits the CDK4/6 kinases and is therefore an important cell cycle regulator. Accumulation of p16INK4A in response to oncogenic transformation leads to cellular senescence and it is therefore frequently lost in cancer. p16INK4A is also known to accumulate under conditions of cellular oxidative stress and therefore could potentially be regulated by redox signaling, which is a form of signal transduction that is mediated by the reversible oxidation of cysteine-thiol side chains in proteins. We found that oxidation of the single cysteine residue in p16INK4A in human cells occurs under relatively mild oxidizing conditions and that this leads to disulfide dependent dimerization. p16INK4A is a well-characterized all alpha-helical protein, but we find that upon cysteine-dependent dimerization, p16INK4A undergoes a dramatic structural rearrangement and forms aggregates that have the typical features of amyloid fibrils, including binding of diagnostic dyes, presence of cross-β sheet structure, and typical dimensions found in electron microscopy. We find that p16INK4A amyloid formation abolishes its function as a CDK4/6 inhibitor in human cells. Taken together, these observations mechanistically link the cellular redox state to the inactivation of p16INK4A through the formation of amyloid fibrils.

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