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The pioneer factor SOX9 competes for epigenetic factors to switch stem cell fates

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE208072 | GEO | 2023/05/05

REPOSITORIES: GEO

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The pioneer factor SOX9 competes for epigenetic factors to switch stem cell fates.

Project description:During development, progenitors simultaneously activate one lineage while silencing another, a feature highly regulated in adult stem cells but derailed in cancers. Equipped to bind cognate motifs in closed chromatin, pioneer factors operate at these crossroads, but how they perform fate switching remains elusive. Here we tackle this question with SOX9, a master regulator that diverts embryonic epidermal stem cells (EpdSCs) into becoming hair follicle stem cells. By engineering mice to re-activate SOX9 in adult EpdSCs, we trigger fate switching. Combining epigenetic, proteomic and functional analyses, we interrogate the ensuing chromatin and transcriptional dynamics, slowed temporally by the mature EpdSC niche microenvironment. We show that as SOX9 binds and opens key hair follicle enhancers de novo in EpdSCs, it simultaneously recruits co-factors away from epidermal enhancers, which are silenced. Unhinged from its normal regulation, sustained SOX9 subsequently activates oncogenic transcriptional regulators that chart the path to cancers typified by constitutive SOX9 expression.

| S-EPMC10415178 | biostudies-literature

The pioneer factor SOX9 competes for epigenetic factors to switch stem cell fates [RNA-Seq]

Project description:When stem cells activate a member of the SOX family of pioneer factors, they bind their cognate sequences within condensed chromatin, not only evicting the associated nucleosome, but also recruiting H3K4-monomethylases, which modify flanking nucleosomes to open chromatin and activate one lineage program; simultaneously, pioneer factors also silence alternative fates, but in this case act indirectly, through competing for H3K4-monomethylases pre-existing at the original fate genes.

2023-05-05 | GSE208071 | GEO