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ATAC-seq changes induced by FOSL1, YAP, and TAZ overexpression in LNCaP Prostate Cancer Cells

ABSTRACT: ATAC-seq changes induced by FOSL1, YAP, and TAZ overexpression in LNCaP Prostate Cancer Cells

PROVIDER: PRJNA819957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18479757_1.fastq.gz	Fastqsanger.gz
	SRR18479757_2.fastq.gz	Fastqsanger.gz
	SRR18479758_1.fastq.gz	Fastqsanger.gz
	SRR18479758_2.fastq.gz	Fastqsanger.gz
	SRR18479759_1.fastq.gz	Fastqsanger.gz

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Gene expression changes induced by FOSL1, YAP, and TAZ overexpression in LNCaP Prostate Cancer Cells

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Gene expression changes induced by FOSL1, YAP, and TAZ overexpression in LNCaP Prostate Cancer Cells

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ChIP-Seq in MSK-PCa3 Prostate Cancer Organoids of FOSL1, TAZ, TEAD1, YAP

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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.

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Characterization of the interactomes of YAP and TAZ in podocytes identifies a relation between YAP and TAZ and proteins of the nuclear shuttling machinery

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