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RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

ABSTRACT: RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

PROVIDER: PRJEB38051 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4078160.fastq.gz	Fastqsanger.gz
	ERR4078161.fastq.gz	Fastqsanger.gz
	ERR4078162.fastq.gz	Fastqsanger.gz
	ERR4078163.fastq.gz	Fastqsanger.gz
	ERR4078158.fastq.gz	Fastqsanger.gz

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RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

Project description:Forelimbs were manually dissected from three individual Bcl9/9l-deltaHD1/deltaHD2 mutants and three control littermates, at 10.5 days post coitum. BCL9 and BCL9L are paralogous beta-catenin cofactors involved in the transcriptional machinery of Wnt target genes.

2020-05-08 | E-MTAB-9000 | biostudies-arrayexpress

ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

Project description:We isolated ca. 500 forelimbs at 10 days post coitum, and performed ChIP-seq using anti-Bcl9 antibodies. Bcl9 is a beta-catenin transcriptional cofactor, therefore it allows the identification of binding sites of the canonical Wnt signalling-dependent transcriptional complex. This experiment allowed to define that, in this developmental context, Bcl9 acts as a beta-catenin dedicated partner. Moreover, it established a series of genome-wide Bcl9 (therefore Wnt/beta-catenin) tissue-specific target loci, thereby assessing the genetic relationship existing between Wnt signaling and other signalling cascades (e.g. the Bmp pathway).

2019-02-21 | E-MTAB-7652 | biostudies-arrayexpress

BCL9/9L-β-catenin Signaling is Associated With Poor Outcome in Colorectal Cancer

Project description:Canonical Wnt signaling output is mediated by β-catenin, which interacts with LEF/TCF transcription factors and recruits a general transcriptional activation complex to its C-terminus. Its N-terminus binds BCL9/9L proteins, which bind co-activators that in mammals contribute to fine-tuning the transcriptional output. We found that a BCL9/9L-dependent gene expression signature was strongly associated with patient outcome in colorectal cancer and that stem cell and mesenchymal genes determine its prognostic value. Abrogating BCL9/9L-β-catenin signaling in independent mouse colorectal cancer models resulted in virtual loss of these traits, and oncogenic intestinal organoids lacking BCL9/9L proteins proved no longer tumorigenic. Our findings suggest that the BCL9/9L arm of Wnt-β-catenin signaling sustains a stemness-to-differentiation equilibrium in colorectal cancer, which critically affects disease outcome. Mutational activation of the Wnt pathway is a key oncogenic event in colorectal cancer. Targeting the pathway downstream of activating mutations is challenging, and the therapeutic window is limited by intestinal toxicity. Contrasting with phenotypes caused by inactivating key Wnt pathway components, ablation of BCL9/9L proteins in adult mice indicated that they were dispensable for intestinal homeostasis, consistent with their role in tuning transcription. Cancer stem cells are increasingly recognized as responsible for tumor recurrence. The correlation between stemness traits in colorectal cancer models and BCL9/9L-β-catenin signaling suggests that high Wnt signaling output is required for their maintenance. Our findings suggest that pruning Wnt-β-catenin signaling might be well tolerated and prove sufficient for trimming stemness traits and improving disease outcome.

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Project description:Bcl9 and Bcl9l (Bcl9l) are commonly thought as beta-catenin-dependent Wnt signaling transcriptional activators. We find however that, in the enamel-producin ameloblasts cells, Bcl9/9l are localiyed in the cytoplasm toward to apical secretory membrane. We performed pull down followed by mass spectrometry analysis to discover the molecular partners of Bcl9 that could explain this cytoplasmic localyzation.

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ChIP-seq experiment of the beta-catenin co-factor BCL9 and the T-box transcription factor TBX3 in developing mouse forelimbs.

Project description:About 500 forelimbs were isolated at 10.5 days post coitum, and ChIP-seq was performed using anti-BCL9 (Abcam, ab37305) and anti-TBX3 (Santacruz, sc17871) antibodies. BCL9 is a beta-catenin transcriptional cofactor involved in the transcriptional machinery of Wnt target genes. TBX3 is a transcription factor important in limb development. This experiment identified, in this developmental context, co-occupancy of BCL9 and TBX3 on a genome-wide scale, and at Wnt-related loci, suggesting co-operation between these transcription factors in Wnt-driven limb development (Zimmerli et al. in revision during spring 2020). The following files are available for this experiment: - Raw sequencing data (.fastq) - Genomic enrichment data in bedgraph format (.bdg) which can be used for visualization in a genome browser. - Annotated peak files (.txt) containing high confidence peaks with genomic annotation. NOTE: The raw data relative to the BCL9 ChIP were previously deposited under accession number E-MTAB-7652, and described in Salazar et al. 2019. For simplicity, and to allow easy retrieval, we add the raw data of the entire experiment (including also BCL9) along with the newly generated analyses.

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BCL9/9L-Î²-catenin Signaling is Associated With Poor Outcome in Colorectal Cancer

Project description:Canonical Wnt signaling output is mediated by Î²-catenin, which interacts with LEF/TCF transcription factors and recruits a general transcriptional activation complex to its C-terminus. Its N-terminus binds BCL9/9L proteins, which bind co-activators that in mammals contribute to fine-tuning the transcriptional output. We found that a BCL9/9L-dependent gene expression signature was strongly associated with patient outcome in colorectal cancer and that stem cell and mesenchymal genes determine its prognostic value. Abrogating BCL9/9L-Î²-catenin signaling in independent mouse colorectal cancer models resulted in virtual loss of these traits, and oncogenic intestinal organoids lacking BCL9/9L proteins proved no longer tumorigenic. Our findings suggest that the BCL9/9L arm of Wnt-Î²-catenin signaling sustains a stemness-to-differentiation equilibrium in colorectal cancer, which critically affects disease outcome. Mutational activation of the Wnt pathway is a key oncogenic event in colorectal cancer. Targeting the pathway downstream of activating mutations is challenging, and the therapeutic window is limited by intestinal toxicity. Contrasting with phenotypes caused by inactivating key Wnt pathway components, ablation of BCL9/9L proteins in adult mice indicated that they were dispensable for intestinal homeostasis, consistent with their role in tuning transcription. Cancer stem cells are increasingly recognized as responsible for tumor recurrence. The correlation between stemness traits in colorectal cancer models and BCL9/9L-Î²-catenin signaling suggests that high Wnt signaling output is required for their maintenance. Our findings suggest that pruning Wnt-Î²-catenin signaling might be well tolerated and prove sufficient for trimming stemness traits and improving disease outcome. Examination of Bcl9/9l-knockout versus wild-type transcriptome in murine AOM-DSS tumors, APC-Kras tumors and healthy colocyte extracts.

2015-11-08 | E-GEOD-60837 | biostudies-arrayexpress

ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

Project description:ChIP-seq experiment of the beta-catenin co-factor Bcl9 in developing forelimbs.

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Project description:RNA-seq experiment of developing mouse forelimbs, comparing Bcl9/9l mutant with control littermates.

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RNAseq of murine small intestinal tissue following epithelium-specific deletion of Bcl9/9l +/- Apc +/- mutant B-catenin

Project description:The aim of this experiment was to determine the contribution that components of the Wnt enhancesome (Bcl9/9l) make to Wnt driven intestinal transcriptional programmes in the context of normal intestinal homeostasis, or intestinal transformation driven by Apc depletion or B-catenin mutation.

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ChIP-seq experiment of the beta-catenin co-factor BCL9 and the T-box transcription factor TBX3 in developing mouse forelimbs.

Project description:ChIP-seq experiment of the beta-catenin co-factor BCL9 and the T-box transcription factor TBX3 in developing mouse forelimbs.

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