Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 8

Similar Datasets

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

Hyperinnervation inhibits organ-level regeneration in mammalian skin

Project description:Hyperinnervation inhibits organ-level regeneration in mammalian skin

| PRJNA1154938 | ENA

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

Hyperinnervation inhibits organ-level regeneration in mammalian skin

Project description:Some mammalian tissues can replace lost cells within one lineage, but organ-level regeneration—restoring diverse cell types across lineages—remains rare. Here we show that late embryonic full-thickness skin injuries heal by regenerating epithelial, mesenchymal, neuronal, and vascular lineages with proper connectivity. However, this ability is lost soon after birth, leading to a failure to restore most cell types and hyperinnervation of the wound bed. Single-cell sequencing identified a postnatal wound-specific fibroblast (PWF) population absent after embryonic wounding. Through an in vivo screen, we discovered three PWF-enriched genes—Timp1, Cxcl12, and Ccl7—that inhibit organ-level regeneration and cause hyperinnervation when overexpressed in embryonic wounds. Reducing hyperinnervation by depleting Cxcl12 in fibroblasts or inhibiting synaptic release enables postnatal skin to regenerate diverse lineages after injury. Our study identifies mechanisms transitioning an organ from regenerative to non-regenerative, discovers fibroblast-driven hyperinnervation as a key barrier, and demonstrates removing this barrier unlocks organ-level regeneration.

2026-03-20 | GSE276119 | GEO

BRD4 promotes endodermal cell fate during mammalian lung development

Project description:BRD4 promotes endodermal cell fate during mammalian lung development

| PRJNA1254236 | ENA

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

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

| PRJNA614521 | ENA

Chromatin state barriers enforce an irreversible mammalian cell fate decision

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

| PRJNA761274 | ENA

Actin and myosin contribute to mammalian mitochondrial DNA maintenance.

Project description: Not available

| S-EPMC3130256 | biostudies-literature

Transcriptomic characterization of Wild type mouse Embryonic Stem Cells (mESCs), β-actin Knock out mESC and upon rescue with a nuclear localization signal β-actin

Project description:Pluripotency and lineage commitment in embryonic stem cells depend on coordinated regulation of chromatin architecture and extracellular matrix (ECM) signaling. Here, we identify nuclear β-actin as a key regulator linking these processes in mouse embryonic stem cells. Loss of β-actin disrupts core pluripotency factors, including Oct4 and Sox2, and causes broad transcriptional changes, while nuclear re-expression rescues these defects. Chromatin accessibility analysis revealed reduced accessibility at regulatory regions of pluripotency genes, consistent with impaired chromatin remodeling. β-actin depletion also altered ECM-related gene expression, matrix properties, and cellular biomechanics, leading to impaired self-renewal, skewed lineage specification, and defective differentiation, particularly reduced neuronal potential and increased mesodermal-like fate bias. In vivo, β-actin loss restricted teratoma growth and compromised tri-lineage differentiation. Together, these results define nuclear β-actin as an important regulator of chromatin accessibility, ECM-dependent signaling, and stem cell fate.

2026-04-13 | GSE327304 | GEO

SETDB1 Regulate Cell State Maintenance and Cell Fate Differentiation in DG

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

| PRJNA1242744 | ENA