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Defining embryo dormancy at single-cell resolution reveals cryptic transcriptional dynamics apace with Yap-mediated mechanotransduction

ABSTRACT: Defining embryo dormancy at single-cell resolution reveals cryptic transcriptional dynamics apace with Yap-mediated mechanotransduction

PROVIDER: PRJNA1008198 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12880038_1.fastq.gz	Fastqsanger.gz
	SRR12880038_2.fastq.gz	Fastqsanger.gz
	SRR12880039_1.fastq.gz	Fastqsanger.gz
	SRR12880039_2.fastq.gz	Fastqsanger.gz
	SRR25734060_1.fastq.gz	Fastqsanger.gz

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Response of podocytes to PAN - YAP-mediated mechanotransduction determines the podocyte's response to damage

Project description:Podocytes are terminally differentiated cells at the kidney filtration barrier and exposed to considerable mechanical strain. Podocyte injury causes morphological changes as a result of cytoskeletal reorganizations and failure of the filtration barrier. The transcriptional co-activators YAP/TAZ are tightly controlled through hippo signaling and responsive to mechanical cues. Here, we show that YAP is upregulated upon podocyte injury to activate YAP-dependent target genes. This activation preceded the development of proteinuria. In contrast, similar perturbations of cells in culture did not reveal increased YAP activity but showed a downregulation of YAP/TAZ activity when cells were grown on stiff surface. However, culture of cells on soft matrix or inhibition of stress fiber formation allowed recapitulation of the damage-induced YAP upregulation indicating a mechanotransduction-dependent mechanism of YAP over-activity. Interestingly, increased expression of YAP targets was confirmed in renal biopsies from patients with glomerular disease. Consistently, pharmacological inhibition of YAP/TEAD activity ameliorated glomerular disease in vivo. These data suggest that perturbation of the mechanosensitive hippo signaling pathway may be a therapeutic principle in podocyte disease.

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Defining embryo dormancy at single-cell resolution reveals cryptic transcriptional dynamics apace with Yap-mediated mechanotransduction

Project description:This SuperSeries is composed of the SubSeries listed below.

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Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction

Project description:Regulation of YAP Promotor Accessibility in Endothelial Mechanotransduction

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CCM3 is a gatekeeper in focal adhesions regulating mechanotransduction and YAP/TAZ signalling

Project description:We report that loss of CCM3/PDCD10 in fibroblasts induces FAK/Src-paxillin signalling driving actomyosin-dependent mechanotransduction leading to YAP/TAZ signalling. In vivo, loss of CCM3 in fibroblasts drives excessive tissue remodelling leading to the dissemination of breast cancer cells to distant organs.

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Caveolin-1 modulates mechanotransduction responses to substrate stiffness through actin-dependent control of YAP

Project description:The transcriptional regulator YAP orchestrates important cell functions, determining tissue homeostasis, organ growth control, and tumorigenesis. Mechanical stimuli are a key input to YAP activity, but the mechanisms controlling this regulation remain largely uncharacterized. We show that CAV1 positively modulates the YAP mechanoresponse to substrate stiffness through actin cytoskeleton-dependent and Hippo kinase-independent mechanisms. RHO activity is necessary but not sufficient for CAV1-dependent mechanoregulation of YAP activity. Systematic quantitative interactomic studies and image-based siRNA screenings provide evidence that this actin-dependent regulation is determined by YAP interaction with the 14-3-3 protein YWHAH. Constitutive YAP activation rescued phenotypes associated with CAV1 loss, including defective ECM remodeling. CAV1-mediated control of YAP activity was validated in vivo in a model of pancreatitis-driven acinar-to-ductal metaplasia. We propose that this CAV1-YAP mechanotransduction system controls a significant share of cell programs linked to these two pivotal regulators, with potentially broad physiological and pathological implications.

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Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [scRNASeq]

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2020-01-13 | GSE138693 | GEO

UPLC-MS/MS of YAP co-IP during activating and inactivating plating conditions

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