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Pioneering function of Yap and Taz in promoting osteogenesis of neural crest cells by preventing chondrogenesis

ABSTRACT: Pioneering function of Yap and Taz in promoting osteogenesis of neural crest cells by preventing chondrogenesis

PROVIDER: PRJNA645902 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12211279_1.fastq.gz	Fastqsanger.gz
	SRR12211279_2.fastq.gz	Fastqsanger.gz
	SRR12211280_1.fastq.gz	Fastqsanger.gz
	SRR12211280_2.fastq.gz	Fastqsanger.gz
	SRR12211281_1.fastq.gz	Fastqsanger.gz

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Pioneering function of Yap and Taz in promoting osteogenesis of neural crest cells by preventing chondrogenesis

Project description:Neural crest cells (NCCs) are multipotent stem cells with a remarkable ability to differentiate into multiple cell lineages, including osteoblasts and chondrocytes. NCCs contribute to the majority of craniofacial skeleton, yet the molecular mechanisms regulating NCCs diversification into osteoblasts or chondrocytes remain poorly understood. We found that Yap and Taz function redundantly as key determinants of the osteogenesis versus chondrogenesis fate decision and differentiation in NCCs in vitro, ex vivo and in vivo, and Yap/Taz-deficiency in NCCs resulted in a switch from osteogenesis to chondrogenesis. Comprehensive analysis of unbiased datasets including CUT&RUN-seq and RNA-seq indicated that Yap/Taz directly regulate key genes that govern osteogenesis and chondrogenesis. During NCC-derived osteogenesis, Yap/Taz promote expression of osteogenic genes such as Runx2 and Sp7 but repress expression of chondrogenic genes such as Sox9 and Col2a1. Further, we found Yap/Taz directly interact with β-catenin in NCCs to coordinately promote osteoblast differentiation and repress chondrogenesis. Together our data indicate that Yap/Taz promote osteogenesis in NCCs by preventing chondrogenesis, partly through interactions with the Wnt-β-catenin pathway.

2022-11-02 | GSE154332 | GEO

Yap and Taz promote osteogenesis and prevent chondrogenesis in neural crest cells in vitro and in vivo.

Project description:Neural crest cells (NCCs) are multipotent stem cells that can differentiate into multiple cell types, including the osteoblasts and chondrocytes, and constitute most of the craniofacial skeleton. Here, we show through in vitro and in vivo studies that the transcriptional regulators Yap and Taz have redundant functions as key determinants of the specification and differentiation of NCCs into osteoblasts or chondrocytes. Primary and cultured NCCs deficient in Yap and Taz switched from osteogenesis to chondrogenesis, and NCC-specific deficiency for Yap and Taz resulted in bone loss and ectopic cartilage in mice. Yap bound to the regulatory elements of key genes that govern osteogenesis and chondrogenesis in NCCs and directly regulated the expression of these genes, some of which also contained binding sites for the TCF/LEF transcription factors that interact with the Wnt effector β-catenin. During differentiation of NCCs in vitro and NCC-derived osteogenesis in vivo, Yap and Taz promoted the expression of osteogenic genes such as Runx2 and Sp7 but repressed the expression of chondrogenic genes such as Sox9 and Col2a1. Furthermore, Yap and Taz interacted with β-catenin in NCCs to coordinately promote osteoblast differentiation and repress chondrogenesis. Together, our data indicate that Yap and Taz promote osteogenesis in NCCs and prevent chondrogenesis, partly through interactions with the Wnt-β-catenin pathway.

| S-EPMC9938793 | biostudies-literature

YAP/TAZ and ATF4 collaboratively drive resistance to Sorafenib therapy in hepatocellular carcinoma by preventing ferroptosis

Project description:Understanding the mechanisms underlying evasive resistance in cancer is an unmet medical need to improve the efficacy of current therapies. In this study, a combination of shRNA-mediated synthetic lethality screening and transcriptomic analysis revealed the transcription factors YAP/TAZ as key drivers of Sorafenib resistance in hepatocellular carcinoma (HCC) by repressing Sorafenib-induced ferroptosis. Mechanistically, in a TEAD-dependent manner YAP/TAZ induce the expression of SLC7A11, a key transporter maintaining intracellular glutathione homeostasis, thus enabling HCC cells to overcome Sorafenib-induced ferroptosis. At the same time, YAP/TAZ sustain the protein stability, nuclear localization and transcriptional activity of ATF4 which in turn cooperates to induce SLC7A11 expression. Our study uncovered a critical role of YAP/TAZ in the repression of ferroptosis and thus in the establishment of Sorafenib resistance in HCC, highlighting YAP/TAZ-based rewiring strategies as potential approaches to overcome HCC therapy resistance.

2021-08-20 | GSE181771 | GEO

Yap/Taz negatively regulate bone angiogenesis and osteogenesis

Project description:In long bone, the metaphyseal region is less hypoxic than the bone marrow (bone shaft). To study the regional differences of vasculatures, we isolated endothelial cells (ECs) expressing membrane-anchored mTomato protein and nuclear H2B-GFP from Cdh5-mT/nG transgenic reporter femoral metaphysis and diaphyseal bone marrow cavity by fluorescence-activated cell sorting (FACS) at high purity for RNA sequencing (RNA-seq). Next, to study the Hippo signaling in bone ECs, we performed RNA-seq analysis of freshly isolated bone ECs from Cdh5Cre-ERT2-positive Yap1/Taz double floxed or Cdh5Cre-ERT2-positive Lats2 floxed allele and their Cre-negative corresponding littermate controls.

2020-01-15 | GSE102181 | GEO

Chondrogenesis in ATDC5 cells

Project description:SAGE analysis of early chondrogenesis in ATDC5 cells induced by BMP4 Keywords: time-course

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ChIP-seq for TAZ (WWTR1) binding region in C2C12 myoblasts

Project description:We demonstrated that TAZ positively regulates Irs1 gene transcription in muscle. Therefore we designed ChIP-seq experiment to reveal detailed mechanism of regulation. To capture TAZ in chromatin preparation, we made Flag-tagged TAZ expressing and control vector transduced C2C12 cells by retroviral infection. We used FLAG-conjugated beads to capture TAZ-chromatin complexes and ChIP-seq was perforemd. Among many TAZ binding sites, we focused Irs1 regulatory region because our primary purpose was to identify TAZ binding site for the regulation of Irs1 transcription.

2018-12-13 | E-MTAB-6764 | biostudies-arrayexpress

Osteogenesis Chip-Seq

Project description:Osteogenesis Chip-Seq

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Osteogenesis RNA-Seq

Project description:Osteogenesis RNA-Seq

| PRJEB4496 | ENA

Chondrogenesis in ATDC5 cells

Project description:SAGE analysis of early chondrogenesis in ATDC5 cells induced by BMP4 Keywords: time-course

2003-09-10 | GSE652 | GEO

YAP/TAZ and ATF4 collaboratively drive resistance to Sorafenib therapy in hepatocellular carcinoma by preventing ferroptosis

Project description:YAP/TAZ and ATF4 collaboratively drive resistance to Sorafenib therapy in hepatocellular carcinoma by preventing ferroptosis