p53-independent apoptosis and p53-dependent block of DNA rereplication following mitotic spindle inhibition in human cells

Exp Cell Res. 1999 Aug 1;250(2):339-50. doi: 10.1006/excr.1999.4554.

Abstract

We have studied the response of human transformed cells to mitotic spindle inhibition. Two paired cell lines, K562 and its parvovirus-resistant KS derivative clone, respectively nonexpressing and expressing p53, were continuously exposed to nocodazole. Apoptotic cells were observed in both lines, indicating that mitotic spindle impairment induced p53-independent apoptosis. After a transient mitotic delay, both cell lines exited mitosis, as revealed by flow-cytometric determination of MPM2 antigen and cyclin B1 expression, coupled to cytogenetic analysis of sister centromere separation. Both cell lines exited mitosis without chromatid segregation. K562 p53-deficient cells further resumed DNA synthesis, giving rise to cells with a DNA content above 4C, and reentered a polyploid cycle. In contrast, KS cells underwent a subsequent G1 arrest in the tetraploid state. Thus, G1 arrest in tetraploid cells requires p53 function in the rereplication checkpoint which prevents the G1/S transition following aberrant mitosis; in contrast, p53 expression is dispensable for triggering the apoptotic response in the absence of mitotic spindle.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Apoptosis* / drug effects
  • Cell Cycle / drug effects
  • Cell Cycle Proteins*
  • Centromere / drug effects
  • Centromere / metabolism
  • Chromosome Segregation / drug effects
  • Cyclin B / analysis
  • Cyclin B1
  • DNA / biosynthesis
  • DNA Fragmentation / drug effects
  • DNA Replication / drug effects
  • DNA Replication / genetics*
  • Dose-Response Relationship, Drug
  • Flow Cytometry
  • Genes, p53*
  • Humans
  • Kinesins
  • Mitotic Index / drug effects
  • Nocodazole / pharmacology
  • Phosphoproteins / analysis
  • Polyploidy
  • Spindle Apparatus / drug effects
  • Spindle Apparatus / physiology*
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / physiology

Substances

  • CCNB1 protein, human
  • Cell Cycle Proteins
  • Cyclin B
  • Cyclin B1
  • Phosphoproteins
  • Tumor Suppressor Protein p53
  • DNA
  • KIF20B protein, human
  • Kinesins
  • Nocodazole