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Canonical WNT signaling-dependent gating of MYC requires a non-canonical CTCF function at a distal binding site

ABSTRACT: Canonical WNT signaling-dependent gating of MYC requires a non-canonical CTCF function at a distal binding site

PROVIDER: PRJNA763189 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15893356_1.fastq.gz	Fastqsanger.gz
	SRR15893356_2.fastq.gz	Fastqsanger.gz
	SRR15893357_1.fastq.gz	Fastqsanger.gz
	SRR15893357_2.fastq.gz	Fastqsanger.gz
	SRR15893358_1.fastq.gz	Fastqsanger.gz

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The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site

Project description:Abnormal WNT signaling increases MYC expression in colon cancer cells in part via oncogenic super-enhancer (OSE)-mediated gating of MYC to the nuclear pore. This process enables MYC transcripts to escape the higher degradation rate in the nucleus compared to the cytoplasm. By targeted mutation, we show here that a single OSE-specific CTCF binding site (CTCFBS) mediates the WNT-regulated increased nuclear export rate of mRNAs derived from its interacting MYC and FAM49B loci, located >0.5 and >2.6 mbp distal of the OSE. The CTCFBS coordinated OSE-MYC proximity with their peripheral localisation, and mediated the WNT-dependent recruitment of the nuclear pore anchor AHCTF1 to the OSE. Furthermore, the CTCFBS up-regulated CCAT1 eRNA transcription, implicated in OSE-MYC interactions, correlating with an enhanced ability of the OSE to reach the nuclear periphery. We submit that WNT-dependent gating of MYC requires CTCF complexed with the OSE to coordinate multiple steps of the gating process.

2021-11-08 | GSE182626 | GEO

Canonical WNT signaling-dependent gating of MYC requires a non-canonical CTCF function at a distal binding site

Project description:Abnormal WNT signaling increases MYC expression in colon cancer cells in part via oncogenic super-enhancer-(OSE)-mediated gating of the active MYC to the nuclear pore in a poorly understood process. We show here that that the principal tenet of the WNT-regulated MYC gating, facilitated nuclear export of the MYC mRNA, converged on a single CTCF binding site (CTCFBS) within the OSE to confer increased growth advantage. To achieve this, the CTCFBS directed in a stepwise manner the WNT-dependent trafficking of the entire OSE to the nuclear pore from intra-nucleoplasmic positions. Once the OSE reached a perinuclear position, triggered by CTCFBS-mediated CCAT1 eRNA activation, its final stretch (<1micrometer) to the nuclear pore required the recruitment of AHCTF1, a key nucleoporin, to the CTCFBS. Thus, a novel WNT-CTCF-eRNA circuit converges on the ability of the OSE to promote pathological cell growth by coordinating the trafficking of MYC within the 3D nuclear architecture.

2021-11-06 | GSE184106 | GEO

The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site

2022-08-31 | GSE182556 | GEO

The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site

Project description:The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site

| PRJNA757124 | ENA

The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site (RNA-Seq II)

2021-11-06 | GSE184103 | GEO

The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site (RNA-Seq II)

Project description:The WNT-dependent gating of MYC requires non-canonical functions of a distal CTCF binding site (RNA-Seq II)

| PRJNA763186 | ENA

Canonical WNT signaling-dependent gating of MYC requires a noncanonical CTCF function at a distal binding site.

Project description:Abnormal WNT signaling increases MYC expression in colon cancer cells in part via oncogenic super-enhancer-(OSE)-mediated gating of the active MYC to the nuclear pore in a poorly understood process. We show here that the principal tenet of the WNT-regulated MYC gating, facilitating nuclear export of the MYC mRNA, is regulated by a CTCF binding site (CTCFBS) within the OSE to confer growth advantage in HCT-116 cells. To achieve this, the CTCFBS directs the WNT-dependent trafficking of the OSE to the nuclear pore from intra-nucleoplasmic positions in a stepwise manner. Once the OSE reaches a peripheral position, which is triggered by a CTCFBS-mediated CCAT1 eRNA activation, its final stretch (≤0.7 μm) to the nuclear pore requires the recruitment of AHCTF1, a key nucleoporin, to the CTCFBS. Thus, a WNT/ß-catenin-AHCTF1-CTCF-eRNA circuit enables the OSE to promote pathological cell growth by coordinating the trafficking of the active MYC gene within the 3D nuclear architecture.

| S-EPMC8752836 | biostudies-literature

ChIP-seq analysis of CTCF in distal limbs at mouse E12.5 using anti-CTCF

Project description:We performed ChIP-seq for CTCF using the autopod from E12.5 embryo and confirmed the binding pattern previously reported by a ChIP-on-Chip approach using the same embryonic tissue (Soshnikova et al., 2010). Our results show CTCF-mediated gating of long-range contacts at the HoxD locus.

2017-07-12 | GSE96558 | GEO

Specification of osteoblast cell fate by canonical Wnt signaling requires Bmp2.

Project description:Enhanced BMP or canonical Wnt (cWnt) signaling are therapeutic strategies employed to enhance bone formation and fracture repair, but the mechanisms each pathway utilizes to specify cell fate of bone-forming osteoblasts remain poorly understood. Among all BMPs expressed in bone, we find that singular deficiency of Bmp2 blocks the ability of cWnt signaling to specify osteoblasts from limb bud or bone marrow progenitors. When exposed to cWnts, Bmp2-deficient cells fail to progress through the Runx2/Osx1 checkpoint and thus do not upregulate multiple genes controlling mineral metabolism in osteoblasts. Cells lacking Bmp2 after induction of Osx1 differentiate normally in response to cWnts, suggesting that pre-Osx1+ osteoprogenitors are an essential source and a target of BMP2. Our analysis furthermore reveals Grainyhead-like 3 (Grhl3) as a transcription factor in the osteoblast gene regulatory network induced during bone development and bone repair, which acts upstream of Osx1 in a BMP2-dependent manner. The Runx2/Osx1 transition therefore receives crucial regulatory inputs from BMP2 that are not compensated for by cWnt signaling, and this is mediated at least in part by induction and activation of Grhl3.

| S-EPMC5201040 | biostudies-literature

Cranial nerve development requires co-ordinated Shh and canonical Wnt signaling.

Project description:Cranial nerves govern sensory and motor information exchange between the brain and tissues of the head and neck. The cranial nerves are derived from two specialized populations of cells, cranial neural crest cells and ectodermal placode cells. Defects in either cell type can result in cranial nerve developmental defects. Although several signaling pathways are known to regulate cranial nerve formation our understanding of how intercellular signaling between neural crest cells and placode cells is coordinated during cranial ganglia morphogenesis is poorly understood. Sonic Hedgehog (Shh) signaling is one key pathway that regulates multiple aspects of craniofacial development, but whether it co-ordinates cranial neural crest cell and placodal cell interactions during cranial ganglia formation remains unclear. In this study we examined a new Patched1 (Ptch1) loss-of-function mouse mutant and characterized the role of Ptch1 in regulating Shh signaling during cranial ganglia development. Ptch1(Wig/ Wig) mutants exhibit elevated Shh signaling in concert with disorganization of the trigeminal and facial nerves. Importantly, we discovered that enhanced Shh signaling suppressed canonical Wnt signaling in the cranial nerve region. This critically affected the survival and migration of cranial neural crest cells and the development of placodal cells as well as the integration between neural crest and placodes. Collectively, our findings highlight a novel and critical role for Shh signaling in cranial nerve development via the cross regulation of canonical Wnt signaling.

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