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Genome wide analysis of binding regions for MYC, MYCN and various histone modifications using Cut&Run

ABSTRACT: Genome wide analysis of binding regions for MYC, MYCN and various histone modifications using Cut&Run

PROVIDER: PRJNA970318 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24474758_1.fastq.gz	Fastqsanger.gz
	SRR24474758_2.fastq.gz	Fastqsanger.gz
	SRR24474759_1.fastq.gz	Fastqsanger.gz
	SRR24474759_2.fastq.gz	Fastqsanger.gz
	SRR24474760_1.fastq.gz	Fastqsanger.gz

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Genome wide analysis of binding regions for MYC, MYCN and various histone modifications using Cut&Run

Project description:Cut&Run analysis was performed in RPMI-8402 cells to analyze binding regions of MYC, MYCN and various histone modifications in normal culture conditions

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Retinoic acid rewires the adrenergic core regulatory circuitry of neuroblastoma but can be subverted by enhancer hijacking of MYC or MYCN (CUT&RUN-Seq)

Project description:Neuroblastoma cell identity depends on a core regulatory circuit (CRC) of transcription factors that incorporate MYCN to drive the oncogenic gene expression program. For neuroblastomas dependent on the adrenergic CRC, treatment with retinoids can inhibit cell growth and induce differentiation in both primary neuroblastomas and cell lines; however, the underlying mechanisms remain unclear. Here we show that when MYCN-amplified neuroblastomas cells are treated with all-trans retinoic acid (ATRA), they undergo modifications of histone H3K27 acetylation and methylation that decommission super-enhancers driving the expression of PHOX2B and GATA3, together with the activation of new super-enhancers that drive high levels of expression of MEIS1, HIC1 and SOX4. These findings indicate that treatment with ATRA can reprogram the enhancer landscape to collapse the adrenergic CRC, which downregulates MYCN expression, while upregulating a new “retino-sympathetic” CRC that causes proliferative arrest and sympathetic differentiation. Thus, we provide mechanisms that account for the beneficial effects of retinoids against high-risk neuroblastoma and explain the rapid downregulation of expression of MYCN despite massive levels of gene amplification.

2021-10-25 | GSE169616 | GEO

CUT&RUN LoV-U of beta-catenin, TCF/LEF transcription factors and histone modifications in HEK293T and mouse embryonic hindlimb tissue at 11.5 days post coitum

Project description:In our attempts to profile different regulators of the WNT/b-catenin transcriptional complex, CUT&RUN failed to produce consistent binding patterns of the non-DNA-binding b-catenin. We developed a modified CUT&RUN protocol, which we refer to as LoV-U (Low Volume and Urea), that enables the generation of robust and reproducible b-catenin binding profiles. CUT&RUN-LoV-U can profile all classes of chromatin regulators tested, as shown by datasets targeting the TCF/LEF transcription factors and various histone modifications. CUT&RUN-LoV-U uncovers direct WNT/β-catenin target genes in human cells, as well as in ex vivo cells isolated from developing mouse tissue.

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