p53 displacement from centrosomes and p53-mediated G1 arrest following transient inhibition of the mitotic spindle.

摘要: Growing evidence indicates a central role for p53 in mediating cell cycle arrest response to mitotic spindle defects so as prevent rereplication cells which the division has failed. Here we report that transient inhibition of assembly induced by nocodazole, tubulin-depolymerizing drug, triggers stable activation p53, can transduce inhibitory signal even when spindle-damaging agent is removed and allowed reassemble. Cells transiently exposed nocodazole continue express high levels p21 follows exposure become arrested G(1), regardless whether they carry diploid or polyploid genome after exit. We also show normally associates with centrosomes cells, whereas disrupts this association. Together these results suggest induction damage, albeit transient, interferes subcellular localization at specific locations, turn dictates offspring such defective mitoses.