Mammalian cells lack checkpoints for tetraploidy, aberrant centrosome number, and cytokinesis failure

摘要: Mammalian cells have been reported to a p53-dependent tetraploidy checkpoint that blocks cell cycle progression in G1 response failure of division. In most cases where the has observed division was perturbed by anti-cytoskeleton drug treatments. However, other evidence argues against existence checkpoint. Cells failed divide differ from normal having two nuclei, centrosomes, decreased surface volume ratio, and undergone an abortive cytokinesis. We tested each these determine which, if any, cause arrest. Primary human diploid fibroblasts with intact checkpoints were used all experiments. Synchronized exhibited arrest caused treatment either cytochalasin or myosin II inhibitor blebbistatin. The role tetraploidy, aberrant centrosome number, increased size cell/cell cell/cytoplast fusion experiments; none conditions resulted Instead we found various treatments cellular damage, which likely When cytokinesis blocked absence damage-inducing no observed. show neither size, nor lead arrest, suggesting there is Rather, certain standard synchronization damage Since tetraploid can when created minimal manipulation, previous reports probably be explained side effects observe them.