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F-actin dynamics regulates mammalian organ growth and cell fate maintenance

ABSTRACT: F-actin dynamics regulates mammalian organ growth and cell fate maintenance

PROVIDER: PRJNA480812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7514411.fastq.gz	Fastqsanger.gz
	SRR7514412.fastq.gz	Fastqsanger.gz
	SRR7514413.fastq.gz	Fastqsanger.gz
	SRR7514414.fastq.gz	Fastqsanger.gz
	SRR7514415.fastq.gz	Fastqsanger.gz

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F-actin dynamics regulates mammalian organ growth and cell fate maintenance

Project description:Cell function depends on the mechanical properties of the microenvironment. Cells probe these features by applying and transmitting forces to their surroundings, via their actomyosin cytoskeleton and adhesion complexes, and then transducing them into biochemical signals. Among these, the transcriptional coactivators YAP/TAZ recently emerged as key factors mediating some biological responses to actomyosin contractility in vitro. However, whether mechanical cues regulate YAP/TAZ activity in vivo, and whether this is relevant for adult tissue homeostasis, remains poorly understood. Here we show that the F-actin capping protein CAPZ is a critical regulator of actomyosin contractility, as its inactivation alters stress fiber and focal adhesion dynamics, leading to enhanced myosin activity and increased cellular traction forces. In vitro, this rescues YAP from inhibition by a small geometry; in vivo, inactivation of Capzb in the mouse liver induces YAP activation and hepatocyte proliferation, leading to striking organ overgrowth. Moreover, Capzb is essential for the maintenance of the differentiated hepatocyte state, and for the metabolic zonation of hepatocytes. In keeping with changes in tissue mechanics and activation of YAP, inhibition of ROCK or deletion of Yap1 reverse the phenotypes emerging in Capzb-null livers. These results indicate a previously unrecognized role for CAPZ in tuning the sensitivity of cells and tissues to mechanical signals, and a physiological function for F-actin dynamics in regulating organ growth and tissue homeostasis.

2019-03-19 | GSE116993 | GEO

RASSF1A IS REQUIRED FOR THE MAINTENANCE OF NUCLEAR ACTIN LEVELS

Project description:Nuclear actin participates in many essential cellular processes including gene transcription, chromatic remodelling and mRNA processing. Actin shuttles into and out the nucleus through the action of dedicated transport receptors importin-9 and exportin-6, but how this transport is regulated remains unclear. Here we show that RASSF1A is a novel regulator of actin nucleocytoplasmic trafficking and is required for the active maintenance of nuclear actin levels through supporting binding of exportin-6 (XPO6) to RAN GTPase. RASSF1A (Ras association domain family 1 isoform A) is a tumor suppressor gene frequently silenced by promoter hypermethylation in all major solid cancers. Specifically, we demonstrate that endogenous RASSF1A localizes to the nuclear envelope (NE) and is required for nucleo-cytoplasmic actin transport and the concomitant regulation of Myocardin-related transcription factor A (MRTF-A), a coactivator of the transcription factor serum response factor (SRF). The RASSF1A/RAN/XPO6/nuclear actin pathway is aberrant in cancer cells where RASSF1A expression is lost and correlates with reduced MTRF/SRF activity leading to cell adhesion defects. Taken together, we have identified a previously unknown mechanism by which the nuclear actin pool is regulated and uncovered a previously unknown link of RASSF1A and MTRF/SRF in tumor suppression.

2019-05-30 | PXD011517 | Pride

Epigenetic control of cellular cross-talk defines organ fate and function

Project description:Epigenetic control of cellular cross-talk defines organ fate and function

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Chromatin state barriers enforce an irreversible mammalian cell fate decision

Project description:Chromatin state barriers enforce an irreversible mammalian cell fate decision

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Actin and myosin contribute to mammalian mitochondrial DNA maintenance.

Project description:Mitochondrial DNA maintenance and segregation are dependent on the actin cytoskeleton in budding yeast. We found two cytoskeletal proteins among six proteins tightly associated with rat liver mitochondrial DNA: non-muscle myosin heavy chain IIA and β-actin. In human cells, transient gene silencing of MYH9 (encoding non-muscle myosin heavy chain IIA), or the closely related MYH10 gene (encoding non-muscle myosin heavy chain IIB), altered the topology and increased the copy number of mitochondrial DNA; and the latter effect was enhanced when both genes were targeted simultaneously. In contrast, genetic ablation of non-muscle myosin IIB was associated with a 60% decrease in mitochondrial DNA copy number in mouse embryonic fibroblasts, compared to control cells. Gene silencing of β-actin also affected mitochondrial DNA copy number and organization. Protease-protection experiments and iodixanol gradient analysis suggest some β-actin and non-muscle myosin heavy chain IIA reside within human mitochondria and confirm that they are associated with mitochondrial DNA. Collectively, these results strongly implicate the actomyosin cytoskeleton in mammalian mitochondrial DNA maintenance.

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SETDB1 Regulate Cell State Maintenance and Cell Fate Differentiation in DG

Project description:SETDB1 Regulate Cell State Maintenance and Cell Fate Differentiation in DG

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Hi-C sequencing analysis of wild-type, β-actin knockout and β-actin hetereozygous mouse embryonic fibroblasts

Project description:β-actin is a crucial component of several chromatin remodeling complexes which control chromatin structure and accessibility. The mammalian Brahma-associated factor (BAF) is one such complex that plays essential roles in development and differentiation by regulating the chromatin state of critical genes and opposing the repressive activity of polycomb repressive complexes. While previous work has shown that β-actin loss can lead to extensive changes in gene expression and heterochromatin organization, it is not known if changes in β-actin levels can directly influence chromatin remodeling activities of BAF and polycomb proteins. Here we conduct a comprehensive genomic analysis of β-actin knockout mouse embryonic fibroblasts (MEFs) using ATAC-Seq, HiC-seq, RNA-Seq and ChIP-Seq of various epigenetic marks. We demonstrate that β-actin levels can affect the complex interplay between chromatin remodelers such as BAF/BRG1 and EZH2 in a dosage-dependent manner. Our results show that changes in β-actin levels and associated chromatin remodeling activities can not only impact local chromatin accessibility but also induce reversable changes in 3D genome architecture. Our findings support a novel role for β-actin levels in shaping the chromatin landscape during development and differentiation.

2021-05-01 | GSE149986 | GEO

ATR-hippo mediates force signalling to nuclear f-actin and links mechanotransduction to neurological disorders.

Project description:The mechanical environment is sensed through cell-matrix contacts with the cytoskeleton, but how signals transit the nuclear envelope to impact cell fate decisions remains unknown. Nuclear actin coordinates chromatin motility during differentiation, plasticity and genome maintenance, yet it also remains unclear how nuclear actin responds to mechanical force. Intriguingly, ATR translocates to the nuclear envelope to protect the nucleus during cell motility or compression. Here, we show that ATR drives nuclear actin assembly via recruitment of Filamin-A to the inner nuclear membrane through binding of the hippo pathway scaffold and ATR-substrate, RASSF1A. Moreover, we demonstrate how germline RASSF1 mutation disables nuclear mechanotransduction resulting in cerebral cortex thinning and associates with common psychological traits. Thus, defective mechanical-regulated pathways may provide an explanation for complex neurological disorders.

2025-05-07 | PXD057905 | Pride

Transcriptional Metabolic Reprograming Drives Meiotic Fate Decision in Mammalian Germ Cells

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Actin binding proteins expression levels when modifying the actin sequence

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