AI Article Synopsis
- DNA methylation plays a vital role in defining cell-type characteristics, but its selective reprogramming during fat cell (adipocyte) development is still not fully understood.
- The study reveals that the transcription factor C/EBPδ and the DNA methylation eraser TET3 work together to regulate adipocyte differentiation by catalyzing DNA demethylation at specific loci.
- This targeted reprogramming enhances the activity of genes related to fat cell development, showing potential in recovering adipogenic ability in aging individuals.
Article Abstract
DNA methylation is a crucial epigenetic modification in the establishment of cell-type-specific characteristics. However, how DNA methylation is selectively reprogrammed at adipocyte-specific loci during adipogenesis remains unclear. Here, we show that the transcription factor, C/EBPδ, and the DNA methylation eraser, TET3, cooperatively control adipocyte differentiation. We perform whole-genome bisulfite sequencing to explore the dynamics and regulatory mechanisms of DNA methylation in adipocyte differentiation. During adipogenesis, DNA methylation selectively decreases at adipocyte-specific loci carrying the C/EBP binding motif, which correlates with the activity of adipogenic promoters and enhancers. Mechanistically, we find that C/EBPδ recruits a DNA methylation eraser, TET3, to catalyse DNA demethylation at the C/EBP binding motif and stimulate the expression of key adipogenic genes. Ectopic expression of TET3 potentiates in vitro and in vivo adipocyte differentiation and recovers downregulated adipogenic potential, which is observed in aged mice and humans. Taken together, our study highlights how targeted reprogramming of DNA methylation through cooperative action of the transcription factor C/EBPδ, and the DNA methylation eraser TET3, controls adipocyte differentiation.
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| http://dx.doi.org/10.1038/s42255-022-00597-7 | DOI Listing |
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