Evidence map›Paper›PMID 41771870›Full record

ArticleNature communications2026

Canonical BAF chromatin remodeling complex specifies stem cell fate via cell-type-specific co-factor recruitment.

Mingyi Zhang, Jifan Feng, Tingwei Guo, Lin Meng, Fei Pei, Lu Gao, Yuchen Yang, Thach-Vu Ho, Yang Chai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Mingyi ZhangCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.
Jifan FengCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.
Tingwei GuoCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.
Lin MengCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-2162-4678
Fei PeiCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-8313-9918
Lu GaoCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.
Yuchen YangCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.
Thach-Vu HoCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA.
Yang ChaiCenter for Craniofacial Molecular Biology, University of Southern California, Los Angeles, CA, USA. [email protected].ORCID http://orcid.org/0000-0003-2477-7247

Funding

MOLECULAR REGULATORY MECHANISM OF MESENCHYMAL STEM CELLS IN ADULT MOUSE INCISORSR01DE025221 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Yang Chai · 2016 to 2026
$4.3M
NIDCR NIH HHS R01 DE025221
6 · The paper itself

Abstract

Individual subunits within the canonical BAF (cBAF) chromatin remodeling complex are known to regulate stem cell behavior, with some functional redundancy across subunits. Yet, how the cBAF complex directs adult stem cell fate specification and maintains stem cell niches remains unclear. Using the adult mouse incisor, we show that cBAF specifies mesenchymal stem cell (MSC) fate by recruiting distinct transcriptional co-factors to shape cell-type-specific chromatin regulation. Through single-cell multi-omics and in vivo functional analyses, we identify ARID1-containing cBAF as an essential gatekeeper that maintains the dynamic balance between MSC self-renewal and differentiation. Specifically, cBAF-DLX2 interactions preserve niche identity by remodeling intronic chromatin accessibility of niche-defining marker Runx2, while cBAF-FOXO1 directly modulates promoter accessibility of lineage-regulating transcription factors, including STAT3 and TRP53, among others, to balance progenitor proliferation and differentiation. Functional perturbation of RUNX2 and TRP53 confirms their roles downstream of cBAF in niche maintenance and fate specification. Our findings establish cBAF as a central regulator of adult stem cell niches and lineage commitment, and highlight cofactor-dependent mechanisms that may have broader implications for tissue regeneration and BAF-associated disorders.

Indexed as

Chromatin Assembly and DisassemblyDNA-Binding ProteinsMesenchymal Stem CellsTranscription FactorsAnimalsCell DifferentiationCell LineageCore Binding Factor Alpha 1 SubunitHomeodomain ProteinsMiceSTAT3 Transcription FactorStem Cell NicheTumor Suppressor Protein p53Arid1a protein, mouseCore Binding Factor Alpha 1 SubunitDNA-Binding ProteinsHomeodomain ProteinsRunx2 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTranscription FactorsTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID41771870
PMCPMC13066034

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.