AI Article Synopsis
- - B23/nucleophosmin moves to spindle poles during metaphase, influenced by exportin Crm1, and plays a role in controlling centrosome duplication.
- - In h-Tert-RPE1 cells, inhibiting Crm1 allows cells to progress to mitosis and leads to the formation of extra spindle poles with gamma-tubulin, NuMA, and B23 despite no change in centrosome number.
- - The study concludes that inhibiting Crm1 during early metaphase promotes the formation of additional spindle poles, but does not affect the total number of centrosomes.
Article Abstract
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 gamma-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.
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| http://dx.doi.org/10.1042/BC20080218 | DOI Listing |
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