Abnormal Centrosome Amplification in the Absence of p53

Abstract

The centrosome plays a vital role in mitotic fidelity, ensuring establishment of bipolar spindles and balanced chromosome segregation. Centrosome duplication occurs only once during the cell cycle and is therefore highly regulated. Here, it is shown that in mouse embryonic fibroblasts (MEFs) lacking the p53 tumor suppressor protein, multiple copies of functionally competent centrosomes are generated during a single cell cycle. In contrast, MEFs prepared from normal mice or mice deficient in the retinoblastoma tumor suppressor gene product do not display these abnormalities. The abnormally amplified centrosomes profoundly affect mitotic fidelity, resulting in unequal segregation of chromosomes. These observations implicate p53 in the regulation of centrosome duplication and suggest one possible mechanism by which the loss of p53 may cause genetic instability.

Keywords

CentrosomeCentrosome cycleMitosisBiologyCell biologySuppressorGene duplicationPLK1Multipolar spindlesChromosome segregationGeneticsCell cycleChromosomeGene

MeSH Terms

AnimalsBloodCellsCulturedCentrosomeCulture MediaFibroblastsGenesRetinoblastomaGenesp53InterphaseMiceMitosisSpindle ApparatusTumor Suppressor Protein p53

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Publication Info

Year: 1996
Type: article
Volume: 271
Issue: 5256
Pages: 1744-1747
Citations: 790
Access: Closed

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APA Style

                            
                                
                                    Kenji Fukasawa, 
                                
                                    Taesaeng Choi, 
                                
                                    Ryoko Kuriyama
                                
                                et al.
                            
                            (1996). 
                            Abnormal Centrosome Amplification in the Absence of p53. 
                            Science
                            , 271
                            (5256)
                            , 1744-1747.
                            https://doi.org/10.1126/science.271.5256.1744
                        

Identifiers

DOI: 10.1126/science.271.5256.1744
PMID: 8596939

Data Quality

Data completeness: 81%