Polo-like Kinase-2 Is Required for Centriole Duplication in Mammalian Cells
| Autor: | Ingrid Hoffmann, Hsiao-Lun Tsai, Silke Warnke, Urs Hoffmann-Rohrer, Andrew M. Fry, Rebecca S. Hames, Stefan Kemmler |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Centriole
Blotting Western Fluorescent Antibody Technique Cell Cycle Proteins Polo-like kinase Protein Serine-Threonine Kinases Xenopus Proteins Biology General Biochemistry Genetics and Molecular Biology 03 medical and health sciences 0302 clinical medicine Cyclin E Animals Humans Protein phosphorylation RNA Small Interfering Kinase activity Cells Cultured Centrioles DNA Primers 030304 developmental biology Centrosome Mammals 0303 health sciences Agricultural and Biological Sciences(all) Biochemistry Genetics and Molecular Biology(all) Kinase Cell Cycle Cyclin-dependent kinase 2 Cell cycle Precipitin Tests Cell biology Gene Expression Regulation 030220 oncology & carcinogenesis biology.protein RNA Interference General Agricultural and Biological Sciences Protein Kinases HeLa Cells Plasmids |
| Zdroj: | Current Biology. 14:1200-1207 |
| ISSN: | 0960-9822 |
| DOI: | 10.1016/j.cub.2004.06.059 |
| Popis: | Centriole duplication initiates at the G1-to-S transition in mammalian cells and is completed during the S and G2 phases. The localization of a number of protein kinases to the centrosome has revealed the importance of protein phosphorylation in controlling the centriole duplication cycle. Here we show that the human Polo-like kinase 2 (Plk2) is activated near the G1-to-S transition of the cell cycle. Endogenous and overexpressed HA-Plk2 localize with centrosomes, and this interaction is independent of Plk2 kinase activity. In contrast, the kinase activity of Plk2 is required for centriole duplication. Overexpression of a kinase-deficient mutant under S-phase arrest blocks centriole duplication. Downregulation of endogenous Plk2 with small hairpin RNAs interferes with the ability to reduplicate centrioles. Furthermore, centrioles failed to duplicate during the cell cycle of human fibroblasts and U2OS cells after overexpression of a Plk2 dominant-negative mutant. These results show that Plk2 is a physiological centrosomal protein and that its kinase activity is likely to be required for centriole duplication near the G1-to-S phase transition. |
| Databáze: | OpenAIRE |
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