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Downstream effects of YAP examined by RNA-Seq analysis of skin in YAP2-5SA-∆C transgenic mice

ABSTRACT: To obtain insights into the global changes of gene expression in the mouse skin in response to epidermal YAP activity, we performed whole transcriptome sequencing of skin tissue of YAP2-5SA-∆C transgenic mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE121194 | GEO | 2018/11/06

REPOSITORIES: GEO

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Downstream effects of YAP examined by RNA-Seq analysis of skin in YAP2-5SA-∆C transgenic mice

Project description:Downstream effects of YAP examined by RNA-Seq analysis of skin in YAP2-5SA-∆C transgenic mice

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Global microRNA expression analysis in mouse skin normal tissues and skin tumors induced by constitutive active YAP mutant.

Project description:Global downregulation of microRNAs (miRNAs) is commonly observed in human cancers and can have a causative role in tumorigenesis. The mechanisms responsible for this phenomenon remain poorly understood. Here we show that YAP, the downstream target of the tumor-suppressive Hippo signaling pathway regulates miRNA biogenesis in a cell density-dependent manner. At low cell density, nuclear YAP binds and sequesters p72 (DDX17), a regulatory component of the miRNA processing machinery. At high cell density, Hippo-mediated cytoplasmic retention of YAP facilitates p72 association with Microprocessor and binding to a specific sequence motif in pri-miRNAs. Inactivation of the Hippo pathway or expression of constitutively active YAP causes widespread miRNA suppression in cells and tumors and a corresponding post-transcriptional induction of MYC expression. Thus, the Hippo pathway links contact-inhibition regulation to miRNA biogenesis and may be responsible for the widespread miRNA repression observed in cancer. Two conditions (normal epidermal cells and oncogenic epidermal cells expressing YAP S127A mutant) were analyzed in duplicate.

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ChIP-seq analysis of MCF10A cells exressing active mutant YAP-5SA

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Project description:We report the gene expression profiles of TRPS-depleted and YAP 5SA overexpressing breast cancer cell lines.

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RNA sequencing of mouse liver cancer cell lines with YAP/TAZ mutations

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RNA-seq on MCF10A-YAP5SA cells (overexpressed constrictively activated YAP in MCF10A cells) transduced with sgRNAs vectors targeting the TEAD4 binding motif within the identified enhancers

Project description:We performed a CRISPR-based functional genetic screen targeting TEAD4 binding motif located within the YAP-bound enhancers. The screen identified seven functional enhancers whose targeting resulted in a marked negative effect on the proliferation of MCF10A-YAP-5SA cells (overexpressed constrictively activated YAP) but no significant effect on MCF10A (parental control) cells. We then carried out RNA-seq analysis on MCF10A-YAP-5SA cells transduced with sgRNA vectors targeting these seven enhancers (enhancers A, B, C, D, E, F, G) as well as the non-targeting sgRNA as control (NT).

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Next Generation Sequencing of first trimester human cytotrophoblasts expressing a constitutively active mutant (5SA) of the transcriptional co-activator YAP.

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Integrin signaling regulates YAP/TAZ to control skin homeostasis

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Discovery of YAP target genes with TNFa or IL-1b induction

Project description:Proper inflammatory responses are vital to restore tissue homeostasis against offending factors. However, it is largely under explored whether inflammatory responses are modulated by the Hippo effectors YAP/TAZ. To identify the transcription targets related to inflammatory reponses for YAP, we utilized human bronchioalveolar carcinoma cells H358 expressing YAP(5SA) or GFP (as a control) and treated with vehicle, TNFa or IL-1b, respectively. Our work disclosed the complex features of YAP/TAZ’s role in inflammatory responses.

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Next Generation Sequencing Identifies Hoxa1 and Hoxc13 as Downstream Targets of Yap in Mouse Epithelial Tissues

Project description:The goals of this study are to identify in vivo downstream targets of Yap through NGS-derived tooth germ transcriptome profiling. The mRNA profiles of wild-type, Yap conditional knockout (CKO) and YAP transgenic (Tg) mouse tooth germs at embryonic day 14.5 were generated by deep sequencing using Illumina Hiseq2000. The sequence reads that passed quality filters were analyzed at the transcript isoform level via DNAnexus. The validation was performed through qRT–PCR and in situ hybrydization. A set of Hox genes were differentially expression in Yap CKO and YAP Tg mouse tooth germs, demonstating concurrent expression changes with Yap transcripts. This study provides a platform to systematically identify in vivo downstream targets of genes of interest. The mRNA profiles of wild type, Yap CKO and YAP Tg mouse tooth germs at embryonic day 14.5 were generated by deep sequencing using Illumina Hiseq.

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