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Incomplete interphase arrest in the G2/M checkpoint of unstressed human cells without centromeric ploidy. G2/M phase arrest has been shown to require a functional centromeres and kinetochores. However, this chromosome condensation-dependent pathway is not always effective. In particular, tumor cells often exhibit an altered G2/M checkpoint. To investigate the mechanism of abnormal G2/M checkpoint of human tumor cells, we have focused on the relationship between a chromosome condensation status of metaphase cells and an activity of the Mad2 protein. We found that the Mad2 protein is localized at centromeres in normal human fibroblasts, whereas it is detected throughout the whole chromosome at the majority of highly polyploid tumor cells. By contrast, Mad2 is detected at the centromeres in a subset of the polyploid tumor cells. These results indicate that the Mad2 protein localization is deregulated during the polyploidization process. Moreover, we showed that the tumor cells whose chromosomes undergo an incomplete interphase arrest with incomplete chromatin condensation arrest at the G2/M checkpoint without a functional centromere in the absence of proper spindle checkpoint function. These observations suggest that the mitotic catastrophe associated with telophase defects might not be due to a lack of G2/M checkpoint control. We discuss the possibility of an alternative mechanism by which a pericentric heterochromatin assembly might cause mitotic catastrophe.

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