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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.

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

PROVIDER: PRJEB38048 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4078121.fastq.gz	Fastqsanger.gz
	ERR4078122.fastq.gz	Fastqsanger.gz
	ERR4078123.fastq.gz	Fastqsanger.gz
	ERR4078124.fastq.gz	Fastqsanger.gz
	ERR4078125.fastq.gz	Fastqsanger.gz

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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.

2020-05-08 | E-MTAB-8997 | 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

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.

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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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A dynamic role of Tbx3 in the pluripotency circuitry

Project description:Pluripotency represents a cell state comprising a fine-tuned pattern of transcription factor activity required for embryonic stem cell (ESC) self-renewal. TBX3 is the earliest expressed member of the T-box transcription factor family and is involved in maintenance and induction of pluripotency. Hence, TBX3 is believed to be a key member of the pluripotency circuitry, with loss of TBX3 coinciding with loss of pluripotency. We report a dynamic expression of TBX3 in vitro and in vivo using genetic reporter tools tracking TBX3 expression in mouse ESCs (mESCs). Low TBX3 levels are associated with reduced pluripotency, resembling the more mature epiblast. Notably, TBX3-low cells maintain the intrinsic capability to switch to a TBX3-high state and vice versa. Additionally, we show TBX3 to be dispensable for induction and maintenance of naive pluripotency as well as for germ cell development. These data highlight novel facets of TBX3 action in mESCs. 12 samples in total

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

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

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Mouse ameloblasts Bcl9 interactors

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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Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis.

Project description:MAPK pathway-driven tumorigenesis, often induced by BRAFV600E, relies on epithelial dedifferentiation. However, how lineage differentiation events are reprogrammed remains unexplored. Here, we demonstrate that proteostatic reactivation of developmental factor, TBX3, accounts for BRAF/MAPK-mediated dedifferentiation and tumorigenesis. During embryonic development, BRAF/MAPK upregulates USP15 to stabilize TBX3, which orchestrates organogenesis by restraining differentiation. The USP15-TBX3 axis is reactivated during tumorigenesis, and Usp15 knockout prohibits BRAFV600E-driven tumor development in a Tbx3-dependent manner. Deleting Tbx3 or Usp15 leads to tumor redifferentiation, which parallels their overdifferentiation tendency during development, exemplified by disrupted thyroid folliculogenesis and elevated differentiation factors such as Tpo, Nis, Tg. The clinical relevance is highlighted in that both USP15 and TBX3 highly correlates with BRAFV600E signature and poor tumor prognosis. Thus, USP15 stabilized TBX3 represents a critical proteostatic mechanism downstream of BRAF/MAPK-directed developmental homeostasis and pathological transformation, supporting that tumorigenesis largely relies on epithelial dedifferentiation achieved via embryonic regulatory program reinitiation.

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Proteostatic reactivation of the developmental transcription factor TBX3 drives BRAF/MAPK-mediated tumorigenesis

2024-02-19 | PXD049704 |