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TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

ABSTRACT: TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

PROVIDER: PRJEB27856 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2708140.fastq.gz	Fastqsanger.gz
	ERR2708141.fastq.gz	Fastqsanger.gz
	ERR2708142.fastq.gz	Fastqsanger.gz
	ERR2708143.fastq.gz	Fastqsanger.gz
	ERR2708144.fastq.gz	Fastqsanger.gz

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TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:During canonical Wnt signalling the activity of nuclear beta-catenin is largely mediated by the TCF/LEF family of transcription factors. To challenge this view we used the CRISPR/Cas9 genome editing approach to generate HEK 293T cell clones simultaneously carrying loss-of-function alleles of all four TCF/LEF genes. Exploiting unbiased whole transcriptome sequencing studies, we found that a subset of beta-catenin transcriptional targets did not require TCF/LEF factors for their regulation. Consistent with this finding, we observed in a genome-wide analysis that beta-catenin occupied specific genomic regions in the absence of TCF/LEF. Finally, we revealed the existence of a transcriptional activity of beta-catenin that specifically appears when TCF/LEF factors are absent, and refer to this as beta-catenin-GHOST response. Collectively, this study uncovers a previously neglected modus operandi of beta-catenin that bypasses the TCF/LEF transcription factors.

2018-11-22 | E-MTAB-7028 | biostudies-arrayexpress

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

2018-11-02 | E-MTAB-7029 | biostudies-arrayexpress

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

| PRJEB27857 | ENA

SOX transcription factors direct TCF-independent Wnt/beta-catenin transcription

Project description:We report ChIP-Seq experiments to profile the genomic binding dynamics of ß-catenin, SOX17, SOX2 and TCF/LEF TFs in definitive endoderm and neuromesodermal progenitor cells and RNA-Seq/ATAC-Seq experiments for transcriptomic and chromatin profiling of these cell types.

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Genome-wide map of Tcf/Lef transcription factors, β-catenin, Six2 and chromatin marks in mouse nephron progenitor cells

Project description:During embryonic kidney development, nephron progenitor cells (NPCs) self-renew and differentiate into all cells in mature nephrons. The Wnt signaling components Wnt9b and β-catenin are required for both NPC self-renewal and differentiation. A low level of Wnt/β-catenin are associated with NPC self-renewal while a high level with differentiation. To investigate the transcriptional mechanisms behind Wnt/β-catenin-driven regulation of NPCs states, we modeled NPC self-renewal and differentiation in vitro with NPEM (Brown et al., 2015) supplemented with low (1.25 μM) or high (5 μM) concentration of CHIR22091 (CHIR), a small molecule GSK3β inhibitor that stabilizes β-catenin. We have found the Tcf/Lef family repressors Tcf7l1 and Tcf7l2 are enriched in low CHIR condition, while the activators Tcf7 and Lef1 in high CHIR condition, correlating with the NPC differentiation program transiting from being repressed to activated. To identify direct transcriptional targets of Tcf/Lef factors and β-catenin, here we generated ChIP-Seq data from primary NPC, as well as NPC cultured in low and high CHIR concentration.

2021-01-07 | GSE131117 | GEO

SOX transcription factors direct TCF-independent Wnt/beta-catenin transcription

Project description:SOX transcription factors direct TCF-independent Wnt/beta-catenin transcription

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ChIP-seq experiment of mouse embryonic stem cells (mESCs), assessing beta-catenin DNA binding in wild type mESCs and TCF/LEF quadruple knock-out mESCs.

Project description:Mouse embryonic stem cells (mESCs), derived from pre-implantation blastocyst cells, can be maintained in vitro in defined N2B27 medium supplemented with two chemical inhibitors for GSK3 and MEK (2i) and the cytokine leukemia inhibitory factor (LIF), which act synergistically to promote self-renewal and pluripotency. Many efforts have been devoted to identify genes that promote exit from the pluripotent state and the transition to a primed state of differentiation. One of the first identified players in this process was the Wnt/b-catenin effector TCF7L1 (previously referred to as TCF3), belonging to the family of four TCF/LEF transcription factors, which acts as pro-differentiation factor by repressing pluripotency genes. Of note, there is little evidence that the genetic abrogation of the mechanisms required for the exit from the pluripotent state is sufficient to enable self-renewal in the absence of 2iL. Here, we found that complete loss-of-function of Tcf7, Lef1, Tcf7l1 and Tcf7l2, the genes encoding for the four TCF/LEF transcription factors, (refered to as qKO) allows mESCs to become fully 2iL-independent and to propagate in basal N2B27. In addition to RNA-seq data deposited under accession number E-MTAB-10564, chromatin immunoprecipitation followed by deep DNA sequencing (ChIP-seq) has been performed in CHIR-stimulated mESCs. Here, the DNA binding landscape of β-catenin has been analyzed to assess its possible connection to TCF/LEF-mediated pluripotency.

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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.

2022-07-16 | E-MTAB-11951 | biostudies-arrayexpress

SPOCK1 activates Wnt/β-Catenin signaling to drive colorectal cancer stemness and progression

Project description:Colorectal cancer (CRC) ranks second in cancer-related mortality worldwide, with clinical intractability and chemoresistance representing significant challenges driven by cancer stem cells (CSCs). Wnt/β-catenin signaling is a lynchpin of CSC self-renewal, but targetable upstream drivers remain elusive. Using bioinformatics we identified the proteoglycan SPOCK1 as a Wnt-associated CSC target. Critically, high SPOCK1 expression predicted poor patient prognosis and reduced progression-free survival following first-line chemotherapy. In vitro assays demonstrated that SPOCK1 levels modulated Wnt/β-catenin activity. SPOCK1 silencing inhibited β-catenin nuclear translocation and TCF/LEF-mediated transcription, which concurrently suppressed CRC proliferation and stemness. Conversely, SPOCK1 overexpression promoted β-catenin nuclear translocation and TCF/LEF-mediated transcription, which enhanced CRC proliferation and stemness. This SPOCK1-driven pro-tumorigenic effect was significantly reversed by the β-catenin/TCF/LEF inhibitor iCRT3, demonstrating SPOCK1’s dependence on Wnt transcriptional activation. The functional role was validated in vivo using a SPOCK1-overexpressing xenograft model and ex vivo using patient-derived organoids (PDOs), both confirming increased growth and β-catenin nuclear localization. Furthermore, data-independent acquisition (DIA) mass spectrometry of SPOCK1-overexpressing tumors revealed pro-tumorigenic signaling including c-Myc activity, oxidative phosphorylation, epithelial-mesenchymal transition. Notably, SPOCK1 drove remodeling of the tumor microenvironment, characterized by desmoplasia and fibrosis. Overall, our findings establish a SPOCK1/Wnt/β-catenin axis as a novel mechanism driving CRC tumorigenesis and stemness, positioning it as a promising therapeutic target to overcome Wnt-mediated progression and resistance.

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