Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Canonical BAF complex orchestrates mesenchymal stem cell niche composition and fate via cofactor-guided chromatin remodeling [CUT&Run]

ABSTRACT: The canonical BAF (BRG1/BRM-associated factor) chromatin remodeling complex plays a pivotal role in governing stem cell behavior, yet how it regulates adult stem cell niche remains unclear. Here, we show that ARID1-containing cBAF complex orchestrates the spatial organization of the mesenchymal stem cell niche and fate in the adult mouse incisor. Dual loss of ARID1A and ARID1B in Gli1+ mesenchymal stem cells using conditional knockout mouse models disturbs chromatin accessibility in a cell-type-specific manner and alters cofactor recruitment, leading to niche cell disorganization, disrupting progenitor cells (transit-amplifying cells, TACs) fate commitment during tissue homeostasis. Single-cell multi-omics profiling and in vivo functional validations reveal that the cBAF complex partners with DLX2 to coordinate niche cell composition and recruits FOXO1 and DLX2 to balance TAC proliferation and differentiation. Our findings establish cBAF as a master regulator of chromatin state and microenvironment architecture, essential for maintaining adult mesenchymal stem cell function and tissue homeostasis.

ORGANISM(S): Mus musculus

PROVIDER: GSE298612 | GEO | 2026/01/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Canonical BAF complex orchestrates mesenchymal stem cell niche composition and fate via cofactor-guided chromatin remodeling [RNA-Seq]

Project description:The canonical BAF (BRG1/BRM-associated factor) chromatin remodeling complex plays a pivotal role in governing stem cell behavior, yet how it regulates adult stem cell niche remains unclear. Here, we show that ARID1-containing cBAF complex orchestrates the spatial organization of the mesenchymal stem cell niche and fate in the adult mouse incisor. Dual loss of ARID1A and ARID1B in Gli1+ mesenchymal stem cells using conditional knockout mouse models disturbs chromatin accessibility in a cell-type-specific manner and alters cofactor recruitment, leading to niche cell disorganization, disrupting progenitor cells (transit-amplifying cells, TACs) fate commitment during tissue homeostasis. Single-cell multi-omics profiling and in vivo functional validations reveal that the cBAF complex partners with DLX2 to coordinate niche cell composition and recruits FOXO1 and DLX2 to balance TAC proliferation and differentiation. Our findings establish cBAF as a master regulator of chromatin state and microenvironment architecture, essential for maintaining adult mesenchymal stem cell function and tissue homeostasis.

2026-01-22 | GSE298610 | GEO

Canonical BAF complex orchestrates mesenchymal stem cell niche composition and fate via cofactor-guided chromatin remodeling [scATAC-seq]

2026-01-22 | GSE298609 | GEO

Canonical BAF complex orchestrates mesenchymal stem cell niche composition and fate via cofactor-guided chromatin remodeling [scRNA-seq]

2026-01-22 | GSE298608 | GEO

Canonical BAF complex orchestrates mesenchymal stem cell niche composition and fate via cofactor-guided chromatin remodeling [CUT&Run DKO]

2026-01-22 | GSE312605 | GEO

Signaling networks of developing hair follicles

Project description:The hair follicle (HF) is a complex miniorgan that serves as an ideal model system to study stem cell (SC) interactions with the niche during growth and regeneration. Dermal papilla (DP) cells are required for activating SCs during the adult hair cycle, but the signal exchange between niche and SC precursors/transit amplifying progenitor cells (TACs) that regulates HF morphogenetic growth is largely unknown. Here we use six transgenic reporters to isolate 14 major skin and HF cell populations. With next-generation RNA sequencing we characterize their transcriptomes and define unique molecular signatures. SC precursors, TACs and the DP niche express a plethora of known and novel ligands and receptors. Signaling interaction network analysis reveals a birds-eye view of pathways implicated in epithelial-mesenchymal interactions. Using a systematic tissue-wide approach this work provides a comprehensive platform, linked to an interactive online database, to identify and further explore the SC/TAC/niche crosstalk regulating HF growth.

2016-03-17 | GSE77197 | GEO

Genome-wide maps of SWI/SNF complexes binding in WT and ARID1-less H2.35 cells

Project description:Globally, the three categories of intact SWI/SNF complexes in control cells have shared and unique binding peaks, with cBAF showing the most abundant binding sites followed by ncBAF and pBAF. In control cells, within cBAF, ARID1B bound to only a subset of ARID1A peaks. In control cells, the binding pattern of BAF45d corresponded to ARID1A patterns, but binding was virtually eliminated in ARID1-less cells. In ARID1-less cells, ARID2 binding was essentially eliminated whereas Brd9 binding was unaltered.

2020-06-10 | GSE140183 | GEO

Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Ring1b ChIP]

Project description:Regulation of transit amplifying cell formation from self-renewing stem cell is fundamental process for cell replacement in a controlled way. Here we analyse the properties of a population of mesenchymal TACs in the continuously growing mouse incisor to identify key components of the molecular regulation that drives proliferation. We show that the polycomb repressive complex 1 acts as a global regulator of the TAC phenotype by its direct action on the expression of key cell cycle regulatory genes and also by regulating Wnt/b-catenin signalling activity. We also identify an essential requirement for TACs in maintaining the mesenchymal stem cells, indicative of a positive feedback mechanism. Analysing the properties of mesenchymal transit amplifying cells population and identifing key components of the molecular regulation that drives proliferation.

2019-03-12 | GSE104892 | GEO

Regulation of mesenchymal stem to transit amplifying cell transition in the continuously growing mouse incisor [Histone ChIP]

2019-03-12 | GSE104891 | GEO

Genome-wide maps of histone modifications unwind in vivo chromatin states of the hair follicle lineage

Project description:Mouse hair follicles (HFs) undergo synchronized cycles. Cyclical regeneration and hair growth is fueled by stem cells (SCs). During the rest phase, the HF-SCs remain quiescent due to extrinsic inhibitory signals within the niche. As activating cues accumulate, HF-SCs become activated, proliferate, and grow downward to form transient-amplifying matrix progenitor cells. We used microarrays to detect the relative levels of global gene expression underlying the states of hair follicle stem cells and their transient-amplifying progeny before differentiation. Quiescent hair follicle stem cells (qHF-SCs), activated hair follicle stem cells (aHF-SCs) and transient-amplifying matrix cells (HF-TACs) were FACS-purified for RNA extraction and hybridization on Affymetrix microarrays. To obtain homogeneous populations of expression profiles, we applied the FACS technique to purify SC and TACs according to their cell surface markers.

2011-09-01 | E-GEOD-31028 | biostudies-arrayexpress

DLX2-FLAG IP-MS in embryonic bodies (EBs): Protein complexes identification

Project description:The ectomesenchyme generates much of the craniofacial skeleton, sutures, and diverse connective tissues in the mammalian head, yet its derivation from embryonic stem cells (ESCs) and the underlying molecular drivers remain poorly defined. Here, we identified Dlx2 as a key regulator that efficiently directed murine ESCs towards Msx1+ ectomesenchyme, recapitulating the developmental trajectory. These Msx1+ progenitors expressed classical craniofacial markers and retained robust osteochondral bipotency in vitro and in vivo. To unravel the molecular machinery, we performed immunoprecipitation mass spectrometry (IP-MS) of DLX2-Flag in ectomesenchymal progenitors, revealing LAP2α as a critical interactor. Mechanistically, DLX2 utilized a lamina-associated polypeptide 2 (LAP2)-dependent nuclear chaperoning system, wherein its 38-amino-acid homeodomain motif directly bound LAP2α. This interaction facilitated nucleosome engagement, chromatin remodeling, and activation of the craniofacial ectomesenchymal gene network. Functional validation showed that disrupting the DLX2-LAP2α interface (via domain deletion or competitive peptides) or silencing Dlx2 targets abolished ectomesenchymal differentiation. Our findings establish DLX2 as a pioneer factor in ectomesenchyme specification, with the DLX2-LAP2α axis serving as a linchpin for chromatin accessibility and lineage commitment, offering insights into craniofacial development and stem cell engineering.

2025-11-06 | PXD064236 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data