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Updated: Jun 15, 2026
14:47
Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
Published on: May 17, 2016
The core binding factor CBF negatively regulates skeletal muscle terminal differentiation.
Ophélie Philipot1, Véronique Joliot, Ouardia Ait-Mohamed
1Institut André Lwoff, FRE2944, CNRS and Université Paris-Sud, Villejuif, France.
Plos One
|March 3, 2010
Summary
Core Binding Factor (CBF) regulates skeletal muscle differentiation. CBFbeta and Runx1 levels control myoblast proliferation and differentiation timing, revealing a new role for CBF in muscle development.
Area of Science:
- Molecular Biology
- Cell Biology
- Developmental Biology
Background:
- Core Binding Factor (CBF) is a transcription factor regulating hematopoiesis.
- CBF consists of Runx1/AML-1 and CBF beta/CBFbeta subunits.
Purpose of the Study:
- Investigate the role of CBF in skeletal muscle terminal differentiation.
- Determine the interaction of CBF with myogenic factors like MyoD.
Main Methods:
- Analyzing protein levels of Runx1 and CBFbeta in myoblasts.
- Studying the effect of CBFbeta overexpression on differentiation.
- Investigating the interaction between CBF and MyoD using co-immunoprecipitation.
- Assessing recruitment of Runx1 to MyoD target genes.
- Analyzing chromatin modifications at MyoD target promoters.
Main Results:
- Downregulation of Runx1 or CBFbeta accelerates skeletal muscle terminal differentiation.
- Overexpression of CBFbeta delays myoblast differentiation.
- CBF directly interacts with MyoD in proliferating myoblasts via Runx1.
- Runx1 is preferentially recruited to MyoD target genes in proliferating myoblasts.
- The MyoD/CBF complex includes chromatin modifiers (HDACs, Suv39h1, HP1beta) that inhibit MyoD activity.
- CBFbeta overexpression leads to increased repressive histone marks and decreased activating marks at MyoD target promoters.
Conclusions:
- Runx1/CBFbeta plays a novel role in controlling skeletal myoblast proliferation and differentiation.
- CBF acts as a regulator of the balance between cell cycle exit and differentiation in skeletal muscle.
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