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Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [ChIP-Seq]

ABSTRACT: The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66081 | GEO | 2015/08/03

SECONDARY ACCESSION(S): PRJNA275844

REPOSITORIES: GEO

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Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [ChIP-Seq]

Project description:The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. ChIP-seq analysis of YAP, TAZ, TEAD4 and JUN in MDA-MB-231 cells. Two independent replicates were analysed for each TF, as well as for negative controls.

2015-08-03 | E-GEOD-66081 | biostudies-arrayexpress

Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [gene expression]

Project description:The goal of this study was to identify YAP/TAZ direct transcriptional targets and transcriptional partners, through ChIP-sequencing and gene expression profiling. Keywords: Expression profiling by array MDA-MB-231 cells growing at low confluence in standard growth conditions were transfected with the indicated siRNAs (Dupont et al., Nature 2011). The following day, growth medium was renewed and cells were incubated for 24 more hours, and then harvested for total RNA extraction. 4 independent biological replicates were plated, transfected and harvested in parallel for each siRNA. Raw .CEL files are the same as in GSE59230 (Enzo et al., EMBO J 2015), but gene expression levels have been quantified using Brainarray HGU133Plus2_Hs_ENTREZG_v17 custom chip definition files.

2015-08-03 | E-GEOD-66082 | biostudies-arrayexpress

Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [gene expression]

2015-08-03 | GSE66082 | GEO

A YAP/TAZ-TEAD signaling module links endothelial nutrient acquisition to angiogenic growth

Project description:Angiogenesis, the process by which endothelial cells (ECs) form new blood vessels from existing ones, is intimately linked to the tissue's metabolic milieu and often occurs at nutrient-deficient sites. However, ECs rely on sufficient metabolic resources to support growth and proliferation. How endothelial nutrient acquisition and usage are regulated is unknown. Here we show that these processes are dictated by YAP/TAZ-TEAD – a transcriptional module whose function is highly responsive to changes in the tissue environment. ECs lacking YAP/TAZ or their transcriptional partners, TEAD1, 2, and 4 fail to divide, resulting in stunted vascular growth in mice. Conversely, activation of TAZ, the more abundant paralogue in ECs, boosts proliferation, leading to vascular hyperplasia. We find that YAP/TAZ promote angiogenesis by fueling nutrient mTORC1 signaling. By orchestrating the transcription of a repertoire of cell-surface transporters, YAP/TAZ-TEAD stimulate the import of amino acids and other essential nutrients, thereby enabling mTORC1 pathway activation. Dissociating mTORC1 from these nutrient inputs – elicited by the loss of Rag GTPases – inhibits mTORC1 activity and prevents YAP/TAZ-dependent vascular growth. These findings define a pivotal role for YAP/TAZ-TEAD in steering endothelial mTORC1 and illustrate the essentiality of coordinated nutrient fluxes in the vasculature.

2022-05-08 | PXD026872 | Pride

Role of YAP/TAZ-TEAD in human trophoblast

Project description:During placentation, placental cytotrophoblast cells differentiate into syncytiotrophoblast cells and extravillous trophoblast cells. In placenta, the expression of various genes is regulated by the Hippo pathway through the transcriptional coactivator YAP/TAZ-TEAD activity. To examine the effect of YAP/TAZ and/or TEAD on trophoblast differentiation, knockdown experiments were performed. Microarray analysis were performed to identify YAP/TAZ and/or TEAD target genes in human trophoblast.

2022-07-17 | GSE182900 | GEO

Genome-wide association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth.

Project description:YAP/TAZ are nuclear effectors of the Hippo pathway regulating organ growth and tumorigenesis. Yet, their function as transcriptional regulators remains underinvestigated. By ChIP-seq analyses in breast cancer cells, we discovered that the YAP/TAZ transcriptional response is pervasively mediated by a dual element: TEAD factors, through which YAP/TAZ bind to DNA, co-occupying chromatin with activator protein-1 (AP-1, dimer of JUN and FOS proteins) at composite cis-regulatory elements harbouring both TEAD and AP-1 motifs. YAP/TAZ/TEAD and AP-1 form a complex that synergistically activates target genes directly involved in the control of S-phase entry and mitosis. This control occurs almost exclusively from distal enhancers that contact target promoters through chromatin looping. YAP/TAZ-induced oncogenic growth is strongly enhanced by gain of AP-1 and severely blunted by its loss. Conversely, AP-1-promoted skin tumorigenesis is prevented in YAP/TAZ conditional knockout mice. This work highlights a new layer of signalling integration, feeding on YAP/TAZ function at the chromatin level.

| S-EPMC6186417 | biostudies-literature

Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-08-03 | GSE66083 | GEO

Transcriptome changes in human endothelial cells with constitutively active YAP, TAZ and TEAD mutants

Project description:Transcriptome profiling of human umbilical vein endothelial cells (HUVECs) overexpressing constitutively nuclear YAP (YAP S127A), TAZ (TAZ S89A) or TEAD-binding deficient YAP (YAP S94A/S127A) or TAZ (TAZ S51A/S89A) to identify YAP and TAZ target genes.

2022-05-02 | GSE163456 | GEO

An allosteric pan-TEAD inhibitor blocks oncogenic YAP/TAZ signaling and overcomes KRAS G12C inhibitor resistance

Project description:The Hippo pathway is a key growth-control pathway conserved across species. The downstream effectors of the Hippo pathway YAP/TAZ are frequently activated in cancer cells by a diverse array of mechanisms to drive proliferation and survival. Based on the premise that sustained interactions between YAP/TAZ and TEADs are central to their transcriptional activities, we discovered a potent small molecule inhibitor (SMI) GNE-7883 that allosterically blocks the interactions between YAP/TAZ and all four TEAD paralogs in human cells through binding to the TEAD lipid pocket. GNE-7883 effectively reduces chromatin accessibility specifically at TEAD motifs, suppresses cell proliferation in a variety of cell line models, and achieved strong anti-tumor efficacy in vivo. Furthermore, we uncovered that GNE-7883 effectively overcomes resistance to the recently approved KRAS G12C inhibitor sotorasib in both treatment-refractory and acquired resistance cell line models, providing strong proof-of-concept of TEAD SMIs in targeting YAP/TAZ-mediated KRAS inhibitor resistance. Taken together, this work demonstrates activities of TEAD SMIs in YAP/TAZ-dependent cancers and highlights their potential broad applications in precision oncology and therapy resistance.

2023-04-26 | GSE229071 | GEO

Yap and Taz regulate retinal pigment epithelial cell fate

Project description:The optic vesicle comprises a pool of bi-potential progenitor cells from which the retinal pigment epithelium (RPE) and neural retina fates segregate during ocular morphogenesis. Several transcription factors and signaling pathways have been shown to be important for RPE maintenance and differentiation, but an understanding of the initial fate specification and determination of this ocular cell type is lacking. We show that Yap/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt RPE identity in zebrafish. A Teadresponsive transgene is expressed within the domain of the optic cup from which RPE arises, and Yap immunoreactivity localizes to the nuclei of prospective RPE cells. yap (yap1) mutants lack a subset of RPE cells and/or exhibit coloboma. Loss of RPE in yap mutants is exacerbated in combination with taz (wwtr1) mutant alleles such that, when Yap and Taz are both absent, optic vesicle progenitor cells completely lose their ability to form RPE. The mechanism of Yap dependent RPE cell type determination is reliant on both nuclear localization of Yap and interaction with a Tead co-factor. In contrast to loss of Yap and Taz, overexpression of either protein within optic vesicle progenitors leads to ectopic pigmentation in a dosagedependent manner. Overall, this study identifies Yap and Taz as key early regulators of RPE genesis and provides a mechanistic framework for understanding the congenital ocular defects of Sveinsson’s chorioretinal atrophy and congenital retinal coloboma. 60 pooled eyes from 36 hpf wild type or vsx2:Gal4/dsRed:14xUAS:YapS87A embryos were pooled for one sample. Three wild type and three vsx2:Gal4/dsRed:14xUAS:YapS87A pools were analyzed for RNA.

2015-08-06 | E-GEOD-71681 | biostudies-arrayexpress

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