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Shared enhancer gene regulatory networks between wound and oncogenic programs

ABSTRACT: Shared enhancer gene regulatory networks between wound and oncogenic programs

PROVIDER: PRJNA844968 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19524300_1.fastq.gz	Fastqsanger.gz
	SRR19524300_2.fastq.gz	Fastqsanger.gz
	SRR19524301_1.fastq.gz	Fastqsanger.gz
	SRR19524301_2.fastq.gz	Fastqsanger.gz
	SRR19524302_1.fastq.gz	Fastqsanger.gz

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Project description:Wound response programs are often activated during neoplastic growth in tumors. In both systems, cells respond to acute stress and balance the activation of multiple programs including apoptosis, proliferation, and cell migration. Central to this response are the JNK/MAPK and JAK/STAT signaling pathways. Yet, to what extent these signaling cascades interact at the cis-regulatory level, and how they orchestrate different phenotypic responses is still unclear. Here, we aim to characterize the cellular states that emerge and cooperate in the wound response, using the Drosophila melanogaster wing disc as a model system. We used single-cell multi-omics profiling to derive enhancer Gene Regulatory Networks (eGRNs) from chromatin accessibility, transcription factor binding motif and gene expression signals. We identify the eGRNs being activated following a transient wound induction, and compare them with the scRNA profiles obtained from a persistent induction of the rasv12 scrib-/- oncogenic driver. We detect a small cell population in the wound that activates a senescence program that is shared with cancer cells. This population is characterized by the C/EBP-like transcription factors Irbp18, Xrp1, slow-border and vrille. Our single-cell multiome and eGRNs resource offers a new perspective on gene regulation in the normal and wounded wing disc.

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Wound epidermis-dependent transcriptional programs

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Shared enhancer gene regulatory networks between wound and oncogenic programs

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

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Wound epidermis-dependent transcriptional programs

Project description:The wound epidermis is required for limb regeneration. To elucidate the roles of the wound epidermis during early regeneration, we examined how the transcriptional programs of early dividing cells (enriched for blastemal progenitors) and non-dividing cells in regenerating stump tissues as well as epithelial cells change when we prevented wound epidermis formation.

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Project description:<p>Metabolic lesions with pleiotropic effects on epigenetic regulation and other cellular processes are widely implicated in cancer, yet their oncogenic mechanisms remain poorly understood. Succinate dehydrogenase (SDH) deficiency causes a subset of gastrointestinal stromal tumors (GISTs) with DNA hyper-methylation. Here we associate this hyper-methylation with changes in chromosome topology that activate oncogenic programs. To investigate epigenetic alterations in this disease, we systematically mapped DNA methylation, CTCF insulators, enhancers and chromosome topology in KIT-mutant, PDGFRA-mutant and SDH-deficient GISTs. Although these respective subtypes share similar enhancer landscapes, we identified hundreds of putative insulators where DNA methylation replaced CTCF binding in SDH-deficient GISTs. We focused on disrupted insulators that partitions super-enhancers from FGF3, FGF4 and the KIT oncogene. Recurrent loss of this insulator alters locus topology in SDH-deficient GISTs, allowing aberrant physical interaction between enhancers and oncogenes. CRISPR-mediated excision of the corresponding CTCF motif in an SDH-intact model disrupted the boundary and up-regulated FGFs and KIT expression. Our findings reveal how a metabolic lesion destabilizes chromatin structure to facilitate the initiation and selection of epigenetic alterations that drive oncogenic programs in the absence of canonical mutations.</p>

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