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Oncogenic YAP mediates changes in chromatin accessibility and activity that drive cell cycle gene expression and cell migration

ABSTRACT: Oncogenic YAP mediates changes in chromatin accessibility and activity that drive cell cycle gene expression and cell migration

PROVIDER: PRJNA797287 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17621334.fastq.gz	Fastqsanger.gz
	SRR17621335.fastq.gz	Fastqsanger.gz
	SRR17621336.fastq.gz	Fastqsanger.gz
	SRR17621337.fastq.gz	Fastqsanger.gz
	SRR17621338.fastq.gz	Fastqsanger.gz

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Oncogenic YAP mediates changes in chromatin accessibility and activity that drive cell cycle gene expression and cell migration

Project description:YAP, the key protein effector of the Hippo pathway, is a transcriptional co-activator that controls the expression of cell cycle genes, promotes cell growth and proliferation and regulates organ size. YAP modulates gene transcription by binding to distal enhancers, but the mechanisms of gene regulation by YAP-bound enhancers remain poorly understood. Here we show that constitutive active YAP5SA leads to widespread changes in chromatin accessibility in untransformed MCF10A cells. Newly accessible regions include YAP-bound enhancers that mediate activation of cycle genes regulated by the Myb-MuvB (MMB) complex. By CRISPR-interference we identify a role for YAP-bound enhancers in phosphorylation of Pol II at Ser5 at MMB-regulated promoters, extending previously published studies that suggested YAP primarily regulates the pause-release step and transcriptional elongation. YAP5SA also leads to less accessible 'closed' chromatin regions, which are not directly YAP-bound but which contain binding motifs for the p53 family of transcription factors. Diminished accessibility at these regions is, at least in part, a consequence of reduced expression and chromatin-binding of the p53 family member ΔNp63 resulting in downregulation of ΔNp63-target genes and promoting YAP-mediated cell migration. In summary, our studies uncover changes in chromatin accessibility and activity that contribute to the oncogenic activities of YAP.

2023-02-15 | GSE193704 | GEO

Oncogenic YAP mediates changes in chromatin accessibility and activity that drive cell cycle gene expression and cell migration.

| S-EPMC10201438 | biostudies-literature

YAP controls cell migration and invasion through a Rho-GTPase switch

Project description:Delineating the mechanisms controlling the invasive spread of non-diseased and transformed cells is central to understanding diverse processes including cancer progression. Here, we found that Yes-associated protein (YAP), a central transcriptional regulator implicated in controlling organ and body size, modulated a Rho-GTPase switch that drives cellular migration by transactivating the Rac1-GEF protein TRIO through direct modulation of its intronic enhancer. Additionally, YAP and TRIO may promote invasive behavior through putative crosstalk with STAT3 signaling, a potential downstream target. Although we found this YAP-dependent infiltrative program in many cell types, it was particularly enhanced in a patient-specific manner in the most common malignant brain tumor, glioblastoma (GBM), where hyperactivation of the YAP, TRIO, and STAT3 signatures also conferred poor clinical outcome. Our analysis suggests that the YAP-TRIO-Rho-GTPase signaling network identified in this study is a ubiquitous regulator of invasive cell spread in both physiological and pathological contexts. In this dataset, we knocked down YAP in two patient-derived GBM primary cell lines (JHGB612 and JHGB651) and performed microarray analysis.

2025-07-23 | GSE289667 | GEO

YAP controls cell migration and invasion through a Rho-GTPase switch

Project description:YAP controls cell migration and invasion through a Rho-GTPase switch

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A Yap-dependent transcriptional program directs cell migration for embryo axis assembly

Project description:The assembly of the embryo’s primary axis is a fundamental landmark to establish the vertebrate body plan. Although the morphogenetic movements directing cell convergence towards the midline have been described extensively, little is known on how gastrulating cells interpret mechanical cues. Yap proteins are well-known transcriptional mechanotransducers, yet their role in gastrulation remains elusive. Here we show that the double knockout of yap and its paralog yap1b in medaka results in an axis assembly failure, due to reduced displacement and migratory persistence in mutant cells. We identified genes involved in cytoskeletal organization and cell-ECM adhesion, rather than in germ layers specification, as direct Yap targets. Dynamic analysis of live sensors and downstream targets reveal that Yap is acting in migratory cells, in which promotes cortical actin and focal adhesions recruitment. Our results indicate that Yap coordinates a mechano-regulatory loop essential to maintain the directed cell migration sustaining embryo axis development.

2022-05-01 | GSE201791 | GEO

YAP regulates cell mechanics by controlling focal adhesion assembly

Project description:Hippo effectors YAP/TAZ act as on-off mechanosensing switches by sensing modifications in extracellular matrix (ECM) composition and mechanics. The regulation of their activity has been described so far through a hierarchical model in which elements of Hippo pathway are under the control of Focal Adhesions (FAs). Here we unveiled the molecular mechanism by which cell spreading and RhoA GTPase control FA formation through YAP to stabilize the anchorage of actin cytoskeleton to cell membrane. This mechanism required YAP co-transcriptional function and involved the activation of genes encoding for integrins and FA docking proteins. Tuning YAP transcriptional activity led to the modification of cell mechanics, force development, adhesion strength, determined cell shaping, migration and differentiation. These results provide new insights into the mechanism of YAP mechanosensing activity and qualify Hippo effector as the key determinant of cell mechanics in response to ECM cues.

2017-05-17 | E-MTAB-5217 | biostudies-arrayexpress

YAP promotes cardiomyocyte cell cycle entry

Project description:YAP promotes cardiomyocyte cell cycle entry

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A Yap-dependent transcriptional program directs cell migration for embryo axis assembly

Project description:A Yap-dependent transcriptional program directs cell migration for embryo axis assembly

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YAP-TEAD multiphasic activation regulates pluripotent stem cell mechanics to drive cardiac specification and contractility in pathological heart.

Project description:YAP transcriptional regulator controls cell mechanics by activating genes involved in cell-matrix interaction following extracellular matrix (ECM) remodelling and stiffening. YAP is needed for cardiogenesis in mouse but is repressed in adult cardiomyocytes. The protein is reactivated following ischemic insults, although the timing and mechanisms underlying YAP depletion during heart development and the reason for its reactivation are unclear. Here, we combine pluripotent stem cell (PSC) cardiac differentiation, mouse embryo development and human heart tissue analysis to demonstrate that the fine-tuning of cell mechanics, as controlled by YAP multiphasic activation through TEAD transcription, is crucial for mesoderm commitment and cardiac progenitor specification. Finally, by adopting induced PSC models of dilated cardiomyopathy, we prove that YAP-TEAD reactivation in diseased cardiomyocytes empowers calcium handling apparatus and increases cell contractility. Given YAP prompt activation following myocardial infarction, we unveil a novel role for mechanosensing in connecting ECM remodelling to cardiomyocyte function in pathological heart.

2020-10-30 | E-MTAB-7619 | biostudies-arrayexpress

YAP-TEAD multiphasic activation regulates pluripotent stem cell mechanics to drive cardiac specification and contractility in pathological heart.

2020-10-30 | E-MTAB-7620 | biostudies-arrayexpress