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An interplay between BRD4 and G9a regulates skeletal myogenesis
Naidi Yang1,2, Dipanwita Das1, Shilpa Rani Shankar1
1Department of Physiology, Healthy Longevity Translational Research Program, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Frontiers in Cell and Developmental Biology
|September 26, 2022
Summary
BRD4 and G9a have opposing roles in muscle cell differentiation. Loss of BRD4 increases G9a activity, impairing muscle development, but inhibiting G9a rescues this defect.
Area of Science:
- Epigenetics
- Molecular Biology
- Cellular Differentiation
Background:
- Histone acetylation and methylation are key epigenetic marks regulating gene expression.
- The coordinated interplay of these marks during cellular differentiation remains incompletely understood.
Purpose of the Study:
- To investigate the relationship between BRD4 (an acetylation reader) and G9a (a methylation writer) in myogenic differentiation.
- To elucidate the mechanism by which BRD4 influences muscle cell development.
Main Methods:
- Loss- and gain-of-function studies were performed for BRD4 and G9a.
- Pharmacological inhibition of G9a methyltransferase activity was employed.
- RNA sequencing was used for transcriptomic analysis.
Main Results:
- BRD4 depletion led to downregulation of myogenic differentiation genes.
- G9a knockdown upregulated some of these same genes, suggesting opposing roles.
- Inhibition of G9a rescued the differentiation defect caused by BRD4 knockdown.
Conclusions:
- BRD4 and G9a exhibit an interdependent relationship in regulating myogenesis.
- Absence of BRD4 leads to increased G9a activity, impairing muscle differentiation.
- This study clarifies the roles of BRD4 and G9a in controlling transcriptional outputs for myogenesis.
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