Abstract

Cell cycle checkpoints enhance genetic fidelity by causing arrest at specific stages of the cell cycle when previous events have not been completed. The tumor suppressor p53 has been implicated in a G1 checkpoint. To investigate whether p53 also participates in a mitotic checkpoint, cultured fibroblasts from p53-deficient mouse embryos were exposed to spindle inhibitors. The fibroblasts underwent multiple rounds of DNA synthesis without completing chromosome segregation, thus forming tetraploid and octaploid cells. Deficiency of p53 was also associated with the development of tetraploidy in vivo. These results suggest that murine p53 is a component of a spindle checkpoint that ensures the maintenance of diploidy.

Keywords

Spindle checkpointCell cycle checkpointG2-M DNA damage checkpointBiologyCell biologyMitosisCell cycleChromosome segregationCHEK1ChromosomeSuppressorSpindle apparatusCancer researchGeneticsCell divisionCellCancerGene

MeSH Terms

AnimalsCell CycleCellsCulturedDNADemecolcineDiploidyFemaleGenesp53MaleMiceMitosisNocodazolePloidiesSpindle ApparatusTumor Suppressor Protein p53

Affiliated Institutions

Related Publications

Publication Info

Year
1995
Type
article
Volume
267
Issue
5202
Pages
1353-1356
Citations
671
Access
Closed

Social Impact

Social media, news, blog, policy document mentions

Citation Metrics

671
OpenAlex
11
Influential
511
CrossRef

Cite This

Shawn M. Cross, Carissa A. Sanchez, Catherine Morgan et al. (1995). A p53-Dependent Mouse Spindle Checkpoint. Science , 267 (5202) , 1353-1356. https://doi.org/10.1126/science.7871434

Identifiers

DOI
10.1126/science.7871434
PMID
7871434

Data Quality

Data completeness: 81%