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USP18 and ISG15 coordinately impact on SKP2 and cell cycle progression
Françoise Vuillier1, Zhi Li1, Pierre-Henri Commere2
1Institut Pasteur, Unit of Cytokine Signaling, Inserm U1221, 75724, Paris, France.
Scientific Reports
|March 13, 2019
Summary
Ubiquitin-specific protease 18 (USP18) and ISG15 regulate S-phase kinase-associated protein 2 (SKP2), impacting cell cycle progression. This interaction stabilizes SKP2, promoting cell division during homeostasis.
Area of Science:
- Molecular Biology
- Cell Biology
- Ubiquitin-Protein Ligase Biology
Background:
- USP18 (Ubiquitin-Specific Protease 18) is an isopeptidase regulating type I interferon signaling by cleaving ISG15 (Interferon-Stimulated Gene 15) from conjugates.
- USP18 protein stability is influenced by ISG15 and targeted for degradation by SKP2 (S-phase Kinase-Associated Protein 2), a component of the SCFSKP2 E3 ubiquitin ligase complex involved in cell cycle progression.
Purpose of the Study:
- To investigate the communication between USP18, ISG15, and SKP2 under non-stimulated conditions.
- To elucidate the regulatory roles of USP18 and ISG15 in SKP2 stability and cell cycle progression.
Main Methods:
- Analysis of protein interactions between USP18 and SKP2.
- Investigation of the effects of ISG15 on the USP18-SKP2 complex.
- Manipulation of USP18 and SKP2 expression levels (enforcing or silencing).
- Assessment of cell cycle progression in HeLa S3 cells with altered USP18 expression.
Main Results:
- USP18 and SKP2 were found to interact, forming a complex.
- Free ISG15 disrupts the USP18-SKP2 complex, leading to USP18 stabilization and SKP2 degradation or ISGylation.
- USP18 was identified as a stabilizer of SKP2, both endogenously and exogenously.
- Silencing of baseline USP18 expression resulted in delayed cell cycle progression of HeLa S3 cells into S phase.
Conclusions:
- USP18 and ISG15 act as novel regulators of SKP2.
- This regulatory axis involving USP18, ISG15, and SKP2 is crucial for maintaining cell cycle progression during cellular homeostasis.
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