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Mouse - Identification of CTNND2 partners in synaptic fractions of P15 mouse brains

ABSTRACT: This project aims to identify CTNND2 partners in developing synapses

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain

SUBMITTER: Vanessa Masson

LAB HEAD: Damarys Loew

PROVIDER: PXD036487 | Pride | 2024-10-03

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	C5348FD.msf	Msf
	C5348FD_30112016.raw	Raw
	C5350FD.msf	Msf
	C5350FD_30112016.raw	Raw
	C6190FD.msf	Msf

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Mouse - SRGAP2 partners in synaptic fractions of P15 mouse brains

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TCF/LEF dependent and independent regulation of 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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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).

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Project description:A comparative ChIP-chip analysis of TFIIB and NC2 in human B cells reveals that basal core promoter architectures control the equilibrium between NC2 and preinitiation complexes. We conducted a comparative ChIP-chip and gene expression analysis of TFIIB in human B cells and analyze associated core promoter architectures. TFIIB occupancy relates well to gene expression, with the vast majority of promoters being GC-rich and lacking defined core promoter elements. TATA consensus and TATA-like motifs but not the previously in vitro defined TFIIB recognition elements (BREs) are enriched in approximately 5% of the genes. Further insight was obtained by performing a parallel ChIP-chip analysis of the TFIIB antagonist NC2. The latter identifies a highly related target gene set. Nonetheless, subpopulations show strong variations in TFIIB/NC2 ratios, with high NC2/TFIIB ratios correlating to promoters that show dispersed transcription start site patterns and lacking defined core elements. Conversely, high TFIIB/NC2 ratios select for conserved core promoter elements that include TATA and INR (initiator), the upstream TFIIB recognition element (BREu) and the downstream promoter element (DPE). Two biological samples from LCL 721 lymphoblastoid human B cells were subjected to ChIP-chip analysis of TFIIB and NC2 using a Nimblegen human promoter array (based on the HG17 genome build) covering 1.5 kb DNA around transcription start sites.

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