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Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
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G1/S Inhibitors and the SWI/SNF Complex Control Cell-Cycle Exit during Muscle Differentiation

Suzan Ruijtenberg1, Sander van den Heuvel1

  • 1Developmental Biology, Department of Biology, Faculty of Sciences, Utrecht University, Padualaan 8, 3584 CH Utrecht, the Netherlands.

Cell
|July 7, 2015
PubMed

Insights

Cell cycle exit during differentiation involves redundant mechanisms. The SWI/SNF complex and G1/S inhibitors provide alternative pathways to arrest cell division, preventing a tumor phenotype.

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Cell-cycle exit is vital for organism development, tissue maintenance, and preventing uncontrolled cell growth.
  • Understanding the molecular mechanisms governing cell-cycle arrest during differentiation is crucial.

Purpose of the Study:

  • To investigate the in vivo mechanisms of cell-cycle exit during differentiation.
  • To identify redundant regulators of cell division arrest.

Main Methods:

  • Development of a conditional knockout and lineage-tracing system in Caenorhabditis elegans.
  • Lineage-specific gene inactivation and genetic screening.
  • Analysis of SWI/SNF chromatin-remodeling complex and G1/S inhibitors.

Main Results:

  • Extensive functional redundancy was found between cell-cycle inhibitors and the SWI/SNF complex.
  • Simultaneous inactivation of SWI/SNF and G1/S inhibitors led to continuous proliferation and a tumor phenotype in C. elegans.
  • SWI/SNF acts with hlh-1 MyoD, antagonizes Polycomb repression, and suppresses cye-1 Cyclin E transcription.

Conclusions:

  • SWI/SNF and G1/S inhibitors offer alternative routes for cell-cycle arrest during terminal differentiation.
  • These findings provide insights into SWI/SNF gene mutations in human cancers.

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