p53 Displacement from Centrosomes and p53-mediated G1 Arrest following Transient Inhibition of the Mitotic Spindle
Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells in which the mitotic division has failed. Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-de...
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| Published in | The Journal of biological chemistry Vol. 276; no. 22; pp. 19205 - 19213 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
01.06.2001
American Society for Biochemistry and Molecular Biology |
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| Abstract | Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells in which the mitotic division has failed. Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-depolymerizing drug, triggers a stable activation of p53, which can transduce a cell cycle inhibitory signal even when the spindle-damaging agent is removed and the spindle is allowed to reassemble. Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G1, regardless of whether they carry a diploid or polyploid genome after mitotic exit. We also show that p53 normally associates with centrosomes in mitotic cells, whereas nocodazole disrupts this association. Together these results suggest that the induction of spindle damage, albeit transient, interferes with the subcellular localization of p53 at specific mitotic locations, which in turn dictates cell cycle arrest in the offspring of such defective mitoses. |
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| AbstractList | Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells in which the mitotic division has failed. Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-depolymerizing drug, triggers a stable activation of p53, which can transduce a cell cycle inhibitory signal even when the spindle-damaging agent is removed and the spindle is allowed to reassemble. Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G(1), regardless of whether they carry a diploid or polyploid genome after mitotic exit. We also show that p53 normally associates with centrosomes in mitotic cells, whereas nocodazole disrupts this association. Together these results suggest that the induction of spindle damage, albeit transient, interferes with the subcellular localization of p53 at specific mitotic locations, which in turn dictates cell cycle arrest in the offspring of such defective mitoses. Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells in which the mitotic division has failed. Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-depolymerizing drug, triggers a stable activation of p53, which can transduce a cell cycle inhibitory signal even when the spindle-damaging agent is removed and the spindle is allowed to reassemble. Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G 1 , regardless of whether they carry a diploid or polyploid genome after mitotic exit. We also show that p53 normally associates with centrosomes in mitotic cells, whereas nocodazole disrupts this association. Together these results suggest that the induction of spindle damage, albeit transient, interferes with the subcellular localization of p53 at specific mitotic locations, which in turn dictates cell cycle arrest in the offspring of such defective mitoses. Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells in which the mitotic division has failed. Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-depolymerizing drug, triggers a stable activation of p53, which can transduce a cell cycle inhibitory signal even when the spindle-damaging agent is removed and the spindle is allowed to reassemble. Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G1, regardless of whether they carry a diploid or polyploid genome after mitotic exit. We also show that p53 normally associates with centrosomes in mitotic cells, whereas nocodazole disrupts this association. Together these results suggest that the induction of spindle damage, albeit transient, interferes with the subcellular localization of p53 at specific mitotic locations, which in turn dictates cell cycle arrest in the offspring of such defective mitoses. |
| Author | Mangiacasale, Rosamaria Soddu, Silvia Ciciarello, Marilena Cundari, Enrico D'Angelo, Marco Casenghi, Martina Lavia, Patrizia Zaira Limongi, Maria |
| Author_xml | – sequence: 1 givenname: Marilena surname: Ciciarello fullname: Ciciarello, Marilena organization: Consiglio Nazionale delle Ricerche Centre of Evolutionary Genetics, Department of Genetics and Molecular Biology, University of Rome “La Sapienza,”; Via degli Apuli 4, Rome 00185, Italy – sequence: 2 givenname: Rosamaria surname: Mangiacasale fullname: Mangiacasale, Rosamaria organization: Consiglio Nazionale delle Ricerche Centre of Evolutionary Genetics, Department of Genetics and Molecular Biology, University of Rome “La Sapienza,”; Via degli Apuli 4, Rome 00185, Italy – sequence: 3 givenname: Martina surname: Casenghi fullname: Casenghi, Martina organization: Consiglio Nazionale delle Ricerche Centre of Evolutionary Genetics, Department of Genetics and Molecular Biology, University of Rome “La Sapienza,”; Via degli Apuli 4, Rome 00185, Italy – sequence: 4 givenname: Maria surname: Zaira Limongi fullname: Zaira Limongi, Maria organization: Consiglio Nazionale delle Ricerche Centre of Evolutionary Genetics, Department of Genetics and Molecular Biology, University of Rome “La Sapienza,”; Via degli Apuli 4, Rome 00185, Italy – sequence: 5 givenname: Marco surname: D'Angelo fullname: D'Angelo, Marco organization: Molecular Oncogenesis Laboratory, Regina Elena Cancer Institute, Rome 00158, Italy – sequence: 6 givenname: Silvia surname: Soddu fullname: Soddu, Silvia organization: Molecular Oncogenesis Laboratory, Regina Elena Cancer Institute, Rome 00158, Italy – sequence: 7 givenname: Patrizia surname: Lavia fullname: Lavia, Patrizia organization: Consiglio Nazionale delle Ricerche Centre of Evolutionary Genetics, Department of Genetics and Molecular Biology, University of Rome “La Sapienza,”; Via degli Apuli 4, Rome 00185, Italy – sequence: 8 givenname: Enrico surname: Cundari fullname: Cundari, Enrico email: ecundari@eudoramail.com organization: Consiglio Nazionale delle Ricerche Centre of Evolutionary Genetics, Department of Genetics and Molecular Biology, University of Rome “La Sapienza,”; Via degli Apuli 4, Rome 00185, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11376010$$D View this record in MEDLINE/PubMed |
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| Snippet | Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells... Growing evidence indicates a central role for p53 in mediating cell cycle arrest in response to mitotic spindle defects so as to prevent rereplication in cells... |
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| StartPage | 19205 |
| SubjectTerms | Anaphase Antineoplastic Agents - pharmacology Blotting, Western Cell Cycle Cell Line Cell Separation Centrosome - metabolism Flow Cytometry Fluorescent Antibody Technique, Indirect G1 Phase Humans K562 Cells Metaphase Microscopy, Fluorescence Mitosis Nocodazole - pharmacology Ploidies Proto-Oncogene Proteins p21(ras) - metabolism Time Factors Transfection Tubulin - metabolism Tumor Suppressor Protein p53 - biosynthesis Tumor Suppressor Protein p53 - metabolism Up-Regulation |
| Title | p53 Displacement from Centrosomes and p53-mediated G1 Arrest following Transient Inhibition of the Mitotic Spindle |
| URI | https://dx.doi.org/10.1074/jbc.M009528200 http://www.jbc.org/content/276/22/19205.abstract https://www.ncbi.nlm.nih.gov/pubmed/11376010 https://search.proquest.com/docview/70879198 |
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