Inhibiting Crm1 causes the formation of excess acentriolar spindle poles containing NuMA and B23, but does not affect centrosome numbers
| Autor: | Annie Rousselet |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Down-Regulation
Receptors Cytoplasmic and Nuclear Cell Cycle Proteins Centrosome cycle Spindle Apparatus Karyopherins Biology Spindle pole body Cell Line Mice Nuclear Matrix-Associated Proteins Animals Humans Centrosome duplication Prometaphase Metaphase Mitosis Centrosome fungi Nuclear Proteins Antigens Nuclear Cell Biology General Medicine Cell biology Protein Transport Nucleophosmin Multipolar spindles |
| Zdroj: | Biology of the Cell. 101:679-693 |
| ISSN: | 0248-4900 |
| DOI: | 10.1042/bc20080218 |
| Popis: | Background. B23/nucleophosmin is present on spindle poles at metaphase. Migration of B23 to the poles is under the control of exportin Crm1. B23 at the centrosome plays a role in the control centrosome duplication. Results. h-Tert-RPE1 cells blocked in prometaphase with low doses of Nocodazol showed a progression to mitosis if Crm1 exportin was inhibited. Under these conditions, the formation of accessory poles containing γ-tubulin, NuMA (nuclear-mitotic-apparatus) and B23 was induced at metaphase. No effect on centrosome number was observed. In quiescent h-Tert-RPE1 cells, when Crm1 was active, B23 was not detected at the centrosome as well as B23-mutants reported to block centrosome duplication. In addition, the modification of B23 nucleo-cytoplasmic shuttling showed no effect on centrosome duplication. Conclusion. Inhibition of Crm1 in early metaphase favours the formation of supplementary acentriolar spindle poles. B23 and NuMA are present at these poles that ultimately focus around the centrosome. Inhibition of Crm1 at metaphase has no effect on the control of centrosome numbers. |
| Databáze: | OpenAIRE |
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