Colony-stimulating factor 1 regulates novel cyclins during the G1 phase of the cell cycle

H Matsushime1, M F Roussel, R A Ashmun

  • 1Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105.

Cell
|May 17, 1991
PubMed

Insights

Colony-stimulating factor 1 (CSF-1) regulates mouse cyclin-like (CYL) gene expression during macrophage G1 phase. CYL proteins are crucial for initiating DNA synthesis, with CSF-1 essential for their stability and function.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Macrophage proliferation is regulated by colony-stimulating factor 1 (CSF-1).
  • Cell cycle progression involves specific gene expression and protein regulation.
  • Cyclin-like (CYL) proteins are implicated in cell cycle control.

Purpose of the Study:

  • To investigate the role of mouse cyclin-like (CYL) genes in macrophage cell cycle regulation.
  • To determine the influence of CSF-1 on CYL gene expression and protein stability.
  • To elucidate the function of CYL proteins during specific cell cycle phases.

Main Methods:

  • Isolation of three mouse CYL genes.
  • Analysis of CYL gene regulation by CSF-1 during the G1 phase.
  • Assessment of CYL protein degradation and phosphorylation.
  • Investigation of CYL protein association with cdc2-related polypeptides.

Main Results:

  • Two of the three isolated CYL genes are regulated by CSF-1 during G1.
  • CSF-1 deprivation in G1 causes rapid degradation of p36CYL proteins.
  • p36CYL degradation correlates with a failure to initiate DNA synthesis.
  • Macrophages entering S phase do not require CSF-1 or CYL gene expression for division.
  • p36CYL is phosphorylated and binds to a cdc2-related polypeptide during G1.

Conclusions:

  • CSF-1 is essential for maintaining CYL protein stability and function during the G1 phase.
  • CYL genes play a critical role in the G1 to S phase transition commitment.
  • The phosphorylation and association of p36CYL with cdc2-related proteins suggest a role in cell cycle regulation.

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