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The lncRNA LUST promotes CCICs self-renewal stimulating the wnt/b-catenin signaling activation

ABSTRACT: The lncRNA LUST promotes CCICs self-renewal stimulating the wnt/b-catenin signaling activation

PROVIDER: PRJNA284938 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2040170_1.fastq.gz	Fastqsanger.gz
	SRR2040170_2.fastq.gz	Fastqsanger.gz
	SRR2040171_1.fastq.gz	Fastqsanger.gz
	SRR2040171_2.fastq.gz	Fastqsanger.gz
	SRR2040172_1.fastq.gz	Fastqsanger.gz

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Canonical Wnt pathway controls mESCs self-renewal through inhibition of spontaneous differentiation via β-catenin/TCF/LEF functions

Project description:The Wnt/β-catenin signalling pathway is a key regulator of embryonic stem cell self-renewal and differentiation. Constitutive activation of this pathway has been shown to significantly increase mouse embryonic stem cell (mESC) self-renewal and pluripotency marker expression. In this study, we generated a novel β-catenin knock-out model in mESCs by using CRISPR/Cas9 technology to delete putatively functional N-terminally truncated isoforms observed in previous knock-out models. While we showed that aberrant N-terminally truncated isoforms are not functional in mESCS, we observed that canonical Wnt signalling is not active in mESCs, as β-catenin ablation does not alter mESC transcriptional profile in LIF-enriched culture conditions; on the other hand, Wnt signalling activation represses mESC spontaneous differentiation. We also showed that transcriptionally silent β-catenin (ΔC) isoforms can rescue β-catenin knock-out self-renewal defects in mESCs, cooperating with TCF1 and LEF1 in the inhibition of mESC spontaneous differentiation in a Gsk3 dependent manner.

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Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway [scRNA-Seq]

Project description:Hematopoietic stem cells (HSCs) have unique abilities to renew themselves and generate differentiated progenies of all blood cell lineages; however, how HSCs maintain the balance of self-renewal and lineage differentiation remains largely unknown. Herein, we showed that in mice the hematologic system deletion of Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b), a protein serine or threonine phosphatase highly expressed in HSCs, induces the suppression of phenotypic HSC expansion due to the blockage of cell cycle. Loss of Ppm1b impairs HSC self-renewal and hematopoietic reconstitution which were revealed by limiting dilution and BM transplantation assays. Through transcriptomic analysis, we observed that the Wnt/β-catenin pathway is downregulated in Ppm1b-deficient mice. Mechanistically, we provided evidence that Ppm1b interacted with β-catenin by performing a proximity ligation assay. Moreover, using an HN252 as a small molecule probe, we further found that Ppm1b inhibition suppressed the self-renewal of HSC and led to a decrease in common lymphoid progenitor cells, resulting in a reduction of B cells in the bone marrow and peripheral blood in turn. In the study we characterized an indispensable role of Ppm1b in regulating HSC self-renewal and B cell development via Wnt/β-catenin pathway.

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Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway [bulk RNA-Seq]

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RNF43 truncations trap CK1 to drive niche-independent self-renewal in cancer

Project description:Wnt/b-catenin signaling is a primary pathway for stem cell maintenance during tissue renewal and a frequent target for mutations in cancer. Impaired Wnt receptor endocytosis due to loss of the ubiquitin ligase RNF43 gives rise to Wnt-hypersensitive tumors that are susceptible to anti-Wnt-based therapy. Contrary to this paradigm, we identify a class of RNF43 truncating cancer mutations that induce b-catenin-mediated transcription, despite exhibiting retained Wnt receptor downregulation. These mutations interfere with an ubiquitin-independent suppressor role of the RNF43 cytosolic tail that involves casein kinase-1 (CK1) binding and phosphorylation. Mechanistically, truncated RNF43 variants trap CK1 at the plasma membrane, thereby preventing b-catenin turnover and propelling ligandindependent target gene transcription. Gene editing of human colon stem cells shows that RNF43 truncations cooperate with p53 loss to drive a niche-independent program for self-renewal and proliferation. Moreover, these RNF43 variants confer decreased sensitivity to anti-Wnt-based therapy. Our data demonstrate the relevance of studying patient-derived mutations for understanding disease mechanisms and improved applications of precision medicine.

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The lncRNA LUST promotes CCICs self-renewal stimulating the wnt/b-catenin signaling activation [RIP-Seq]

Project description:Comprehensive RNA-seq experiments in CD24bright/CD44bright (CCICs), CD24dim/CD44dim (more differentiated counterpart) cells and colonospheres delineate the role of the lncRNA LUST in promoting CCICs self-renewal

2016-05-25 | GSE69234 | GEO

The lncRNA LUST promotes CCICs self-renewal stimulating the wnt/b-catenin signaling activation [RNA-Seq]

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A Glis3-CD133-Wnt signaling axis regulating the self-renewal of adult murine pancreatic progenitor-like cells in colonies/organoids

Project description:Adult pancreatic progenitor cells are a potential source of renewable insulin producing cells that can be used in regenerative medicine and cell replacement therapy for type-1 diabetes. We sought to understand the mechanisms by which adult pancreatic progenitor cells undergo self-renewal. The effects of knockdown of Glis3, CD133 (Prominin-1) and beta-catenin were investigated and we found that Glis3 and CD133 are capable of regulating self-renewal through Wnt gene expression.

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Canonical Wnt pathway controls mESCs self-renewal through inhibition of spontaneous differentiation via β-catenin/TCF/LEF functions

Project description:Canonical Wnt pathway controls mESCs self-renewal through inhibition of spontaneous differentiation via β-catenin/TCF/LEF functions

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Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway

Project description:Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway

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FGF-WNT omic correlation project

Project description:Both FGF and WNT pathways play important roles in embryonic development, stem cell self-renewal and are frequently deregulated in breast cancer. To study the cooperation between FGF and WNT signaling, we have generated a mouse model, MMTV-WNT1/MMTV-iFGFR1 (WNT/iR1), in which we could chemically overactivate iFGFR1 in a ligand-independent manner.

2017-11-22 | MSV000081730 | MassIVE

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