Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA317776 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3350960_1.fastq.gz | Fastqsanger.gz | |||
| SRR3350960_2.fastq.gz | Fastqsanger.gz | |||
| SRR3350970_1.fastq.gz | Fastqsanger.gz | |||
| SRR3350970_2.fastq.gz | Fastqsanger.gz | |||
| SRR3350961_1.fastq.gz | Fastqsanger.gz |
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Project description:The Hippo pathway plays a crucial in organ size control during development and tissue homeostasis in adult life. To examine a role for Hippo signaling in the intestinal epithelium, we analyzed gene expression patterns in the mouse intestinal epithelilum transfected with siRNAs or expression plasmids for shRNAs targeting the Hippo pathway effectors, YAP and TAZ. We performed two independent series of experiments (siGFP (n=3) vs siYAP/siTAZ (n=3), and shLacZ (n=1) vs shYAP/shTAZ (n=1)). Control siRNA (siGFP), YAP/TAZ siRNAs, or expression plasmids for control shRNA (shLacZ) or YAP/TAZ shRNAs were introduced into the mouse intestinal epithelium by the newly-developed in vivo transfection method. Four days after transfection, intestinal epithelial cells were isolated from the tissues and total RNA was extracted.
2014-07-18 | E-GEOD-45155 | biostudies-arrayexpress
Project description:The skin is a squamous epithelium that is continuously renewed by a population of basal layer stem/progenitor cells and can heal wounds. Here, we show that the transcription regulators YAP and TAZ localise to the nucleus in the basal layer of skin and are elevated upon wound healing. Skin-specific deletion of both YAP and TAZ in adult mice slows proliferation of basal layer cells, leads to hair loss and impairs regeneration after wounding. Contact with the basal extracellular matrix and consequent integrin-Src signalling is a key determinant of the nuclear localisation of YAP/TAZ in basal layer cells and in skin tumours. Contact with the basement membrane is lost in differentiating daughter cells, where YAP and TAZ become mostly cytoplasmic. In other types of squamous epithelia and squamous cell carcinomas, a similar control mechanism is present. By contrast, columnar epithelia differentiate an apical domain that recruits CRB3, Merlin (also known as NF2), KIBRA (also known as WWC1) and SAV1 to induce Hippo signalling and retain YAP/TAZ in the cytoplasm despite contact with the basal layer extracellular matrix. When columnar epithelial tumours lose their apical domain and become invasive, YAP/TAZ becomes nuclear and tumour growth becomes sensitive to the Src inhibitor Dasatinib.
2016-04-09 | GSE80082 | GEO
Project description:The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
2025-12-16 | GSE277190 | GEO
Project description:The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
2025-12-16 | GSE277189 | GEO
Project description:The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
2025-12-16 | GSE277188 | GEO
Project description:The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
2025-12-16 | GSE277187 | GEO
Project description:The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
2025-12-16 | GSE252503 | GEO
Project description:The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
2025-12-16 | GSE248364 | GEO
Project description:Uncontrolled Transforming growth factor-beta (TGFβ) signaling promotes aggressive metastatic properties in late-stage breast cancers. However, how TGFβ-mediated cues are directed to induce late-stage tumorigenic events is poorly understood, particularly given that TGFβ has clear tumor suppressing activity in other contexts. Here we demonstrate that the transcriptional regulators TAZ and YAP (TAZ/YAP), key effectors of the Hippo pathway, are necessary to promote and maintain TGFβ-induced tumorigenic phenotypes in breast cancer cells. Interactions between TAZ/YAP, TGFβ-activated SMAD2/3, and TEAD transcription factors reveal convergent roles for these factors in the nucleus. Genome-wide expression analyses indicate that TAZ/YAP, TEADs and TGFβ-induced signals coordinate a specific pro-tumorigenic transcriptional program. Importantly, genes cooperatively regulated by TAZ/YAP, TEAD, and TGFβ, such as the novel targets NEGR1 and UCA1, are necessary for maintaining tumorigenic activity in metastatic breast cancer cells. Nuclear TAZ/YAP also cooperate with TGFβ signaling to promote phenotypic and transcriptional changes in non-tumorigenic cells to overcome TGFβ repressive effects. Our work thus identifies crosstalk between nuclear TAZ/YAP and TGFβ signaling in breast cancer cells, revealing novel insight into late-stage disease-driving mechanisms. Expression profiling was conducted following the repression of the transcriptional regulators TAZ and YAP (TAZ/YAP), the TEAD family of transcription factors (TEAD1/2/3/4), or the TGFb signaling pathway (with SB-431542, an inhibitor of the TBRI recpeptor) in human MDA-MB-231-LM2 breast cancer cells treated with TGFβ1. Human MDA-MB-231-LM2-4 breast cancer cells were transfected with control siRNA, or siRNAs targeting TAZ/YAP or all four TEADs and were treated 24 hours later with 500pM TGFβ1 or 5mM SB-431542 for an additional 24 hours. Total RNA was isolated and twelve microarrays in total were performed, with each condition carried out three times on separate days. The Boston University Microarray Core generated the data using the Affymetrix Human Gene 1.0 St Array.
2014-04-02 | E-GEOD-56445 | biostudies-arrayexpress
Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. In this study we have described essential roles for the transcriptional regulators YAP and TAZ, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. Lineage specific deletion of Yap and Taz in Scgb1a1+ cells leads to increased Mucin production within the knockout cells in vivo. In order better characterize the in vivo transcriptional changes associated with Yap/Taz knockout in these cells, we have isolated Scgb1a1 lineage traced cells from control and yap/taz cNull mice and performed bulk RNA sequencing.
2021-08-09 | GSE171712 | GEO