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Decoding the YAP/TAZ–PPARγ Regulatory Axis in Adipocyte Differentiation and Dedifferentiation [CUT&Tag]

GSE277187 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2025/12/16 Platform GPL24247
Summary
The transcriptional coregulators YAP and TAZ control tissue homeostasis as downstream effectors of the Hippo signaling pathway. The molecular mechanisms by which they regulate cell differentiation or dedifferentiation have remained unclear, however. Here we reveal how YAP/TAZ regulates the transcription and genomic activity of the adipocyte lineage-specification factor PPARγ at the chromatin level. TAZ binds to the Pparg2 genomic region and to PPARγ target gene enhancers, thereby inducing chromatin reprogramming and transcriptional repression. Binding to TEAD transcription factors is essential for this repressive action of TAZ, but direct protein interaction with PPARγ via the WW domain of TAZ is not. Single-nucleus genomic analyses of mouse adipose tissue revealed that YAP/TAZ hyperactivation drives extensive epigenetic changes and the dedifferentiation of adipocytes. Collectively, our findings indicate that YAP/TAZ determine adipocyte fate by modulating the expression of a key transcription factor and the enhancer landscape of its target genes.
Published in
YAP/TAZ-VGLL3 governs adipocyte fate via epigenetic reprogramming of PPARγ and its target enhancers
Seol T, Kang JG, Ryu K et al. · Science advances 2026 · PMID 41533786 · doi:10.1126/sciadv.aea7235
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Also filed as BioProject PRJNA1161161 and SRA study SRP532733. Searching any of these in the dataset finder brings you back here.

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