Multipolar mitosis of tetraploid cells: Inhibition by p53 and dependency on Mos Academic Article uri icon

Overview

MeSH Major

  • Carcinoma
  • Colonic Neoplasms
  • Genes, mos
  • Mitosis
  • Polyploidy
  • Tumor Suppressor Protein p53

abstract

  • Tetraploidy can constitute a metastable intermediate between normal diploidy and oncogenic aneuploidy. Here, we show that the absence of p53 is not only permissive for the survival but also for multipolar asymmetric divisions of tetraploid cells, which lead to the generation of aneuploid cells with a near-to-diploid chromosome content. Multipolar mitoses (which reduce the tetraploid genome to a sub-tetraploid state) are more frequent when p53 is downregulated and the product of the Mos oncogene is upregulated. Mos inhibits the coalescence of supernumerary centrosomes that allow for normal bipolar mitoses of tetraploid cells. In the absence of p53, Mos knockdown prevents multipolar mitoses and exerts genome-stabilizing effects. These results elucidate the mechanisms through which asymmetric cell division drives chromosomal instability in tetraploid cells.

publication date

  • April 2010

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2857458

Digital Object Identifier (DOI)

  • 10.1038/emboj.2010.11

PubMed ID

  • 20186124

Additional Document Info

start page

  • 1272

end page

  • 84

volume

  • 29

number

  • 7