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Loss of the mammalian DREAM complex deregulates chondrocyte proliferation

Chantal Forristal1, Shauna A Henley1, James I MacDonald1

  • 1London Regional Cancer Program, Western University, London, Ontario, Canada Department of Biochemistry, Western University, London, Ontario, Canada.

Molecular and Cellular Biology
|April 9, 2014
PubMed

Insights

Mammalian DREAM complex deficiency prevents cell cycle exit in chondrocytes, leading to failed bone formation and early death. This highlights DREAM

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • The DREAM complex is crucial for cellular quiescence, comprising E2F, RB-family proteins, and the MuvB core.
  • MuvB can alternatively bind BMYB to promote proliferation, complicating studies of DREAM function.
  • Understanding DREAM's role in cell cycle regulation is essential for developmental processes.

Purpose of the Study:

  • To investigate the function of the DREAM complex in mammalian cellular quiescence and development.
  • To elucidate the role of DREAM complex assembly in preventing uncontrolled cell proliferation.
  • To determine the necessity of DREAM for proper endochondral bone formation.

Main Methods:

  • Generated a gene-targeted mouse model deficient for DREAM complex assembly by targeting p107 and p130.
  • Utilized micro-computed tomography and histology to analyze bone development defects.
  • Employed embryonic bone culture and DYRK1A kinase inhibition to study DREAM assembly requirements.

Main Results:

  • DREAM-deficient mice exhibit preferential BMYB-MuvB complex assembly, leading to transcriptional dysregulation.
  • These mice display severe defects in endochondral bone formation and perinatal lethality.
  • Chondrocytes in DREAM-deficient mice fail to arrest proliferation, indicating a role in cell cycle exit.

Conclusions:

  • Mammalian DREAM complex assembly is essential for inducing cell cycle exit in chondrocytes.
  • Deficiency in DREAM leads to impaired endochondral ossification due to persistent chondrocyte proliferation.
  • DYRK1A-mediated phosphorylation of LIN52 is critical for DREAM assembly and its function in development.

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