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Published on: February 20, 2018
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.
Abstract:
Three mouse cyclin-like (CYL) genes were isolated, two of which are regulated by colony-stimulating factor 1 (CSF-1) during the G1 phase of the macrophage cell cycle. CSF-1 deprivation during G1 leads to rapid degradation of CYL proteins (p36CYL) and correlates with failure to initiate DNA synthesis. However, after entering S phase, macrophages no longer require CSF-1 and can complete cell division without expressing CYL genes. During G1, p36CYL is phosphorylated and associates with a polypeptide antigenically related to p34cdc2. The timing of p36CYL expression, its rapid turnover in the absence of CSF-1, and its phosphorylation and transient binding to a cdc2-related polypeptide suggest that CYL genes may function during S phase commitment.
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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