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Prmt6 represses the pro-adipogenic Ppar-gamma-C/ebp-alpha transcription factor loop.
Mirjam Gerstner1, Vivien Heller1, Johannes Fechner1
1Department of Eukaryotic Genetics, Institute of Biomedical Genetics, University of Stuttgart, Allmandring 31, 70569, Stuttgart, Germany.
Scientific Reports
|March 21, 2024
Summary
The feed-forward loop involving Ppar-gamma and C/ebp-alpha is key for adipocyte differentiation. Prmt6 epigenetic factor represses this loop, and its inhibition promotes adipogenesis.
Area of Science:
- Epigenetics
- Molecular Biology
- Cell Differentiation
Background:
- The Ppar-gamma and C/ebp-alpha feed-forward loop is crucial for adipocyte differentiation.
- Epigenetic cofactors interacting with Ppar-gamma are central to understanding adipogenesis in health and disease.
Purpose of the Study:
- To investigate the role of the epigenetic factor Prmt6 in the Ppar-gamma and C/ebp-alpha regulatory loop.
- To elucidate the molecular mechanisms underlying adipocyte differentiation and identify potential therapeutic targets.
Main Methods:
- Chromatin immunoprecipitation to identify Prmt6 binding sites.
- Quantitative real-time PCR to assess gene expression.
- Histone modification analysis (H3R2me2a).
- Pharmacological inhibition of Prmt6.
Main Results:
- Prmt6 was found to bind the Ppar-gamma and C/ebp-alpha promoter, repressing C/ebp-alpha expression via H3R2me2a induction.
- Prmt6 expression decreased during adipocyte differentiation, leading to Ppar-gamma and C/ebp-alpha upregulation.
- Small molecule inhibition of Prmt6 enhanced adipogenesis.
Conclusions:
- Prmt6 acts as a negative regulator in the Ppar-gamma-C/ebp-alpha feed-forward loop during adipogenesis.
- Inhibiting Prmt6 offers a potential strategy for epigenetic manipulation of adipocyte differentiation.
- This study provides mechanistic insights into normal and aberrant adipogenesis.
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