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Chd2 interacts with H3.3 to determine myogenic cell fate
Akihito Harada1, Seiji Okada, Daijiro Konno
1Department of Advanced Medical Initiatives, JST-CREST, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
The EMBO Journal
|May 10, 2012
Summary
Chromodomain helicase DNA-binding domain 2 (Chd2) facilitates cell differentiation by depositing histone variant H3.3 at specific gene loci. This Chd2-dependent process is crucial for activating myogenic genes and determining cell fate.
Area of Science:
- Molecular Biology
- Epigenetics
- Cell Biology
Background:
- Cell differentiation relies on lineage-determining transcription factors.
- Chromatin remodelling enzymes play key roles in regulating gene expression during differentiation.
Purpose of the Study:
- To investigate the role of chromodomain helicase DNA-binding domain 2 (Chd2) in cell differentiation.
- To elucidate the mechanism by which Chd2 influences myogenic gene activation and histone variant deposition.
Main Methods:
- Interaction studies between Chd2, MyoD, and myogenic gene regulatory sequences.
- Analysis of H3.3 histone variant deposition at specific loci using directed and genome-wide approaches.
- Chd2 knockdown experiments to assess the impact on H3.3 incorporation and gene activation.
Main Results:
- Chd2 interacts with MyoD and myogenic loci, mediating H3.3 deposition prior to differentiation.
- Chd2 knockdown inhibits H3.3 deposition at differentiation-dependent genes but not housekeeping genes.
- Chd2 knockdown impairs myogenic gene activation, indicating its essential role in the differentiation process.
Conclusions:
- MyoD determines cell fate and drives differentiation-dependent gene expression.
- Chd2 facilitates MyoD's function through the deposition of H3.3 at myogenic loci.
- Chd2-mediated H3.3 deposition is a critical epigenetic event preceding cell differentiation.
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