Programmed Cell Death and Bcl-2 Protection in the Absence of a Nucleus

EMBO J. 1994 Apr 15;13(8):1899-910.

Abstract

The molecular basis of programmed cell death (PCD) is unknown. An important clue is provided by the Bcl-2 protein, which can protect many cell types from PCD, although it is not known where or how it acts. Nuclear condensation, DNA fragmentation and a requirement for new RNA and protein synthesis are often considered hallmarks of PCD. We show here, however, that anucleate cytoplasts can undergo PCD and that Bcl-2 and extracellular survival signals can protect them, indicating that, in some cases at least, the nucleus is not required for PCD or for Bcl-2 or survival factor protection. We propose that PCD, like the cell cycle, is orchestrated by a cytoplasmic regulator that has multiple intracellular targets.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkaloids / pharmacology
  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / physiology*
  • Cell Nucleus / physiology*
  • Cytoplasm / physiology*
  • Fibroblasts / drug effects
  • Fibroblasts / physiology
  • Growth Substances / pharmacology
  • Humans
  • Models, Biological
  • Oligodendroglia / drug effects
  • Oligodendroglia / physiology
  • Protein Synthesis Inhibitors / pharmacology
  • Proto-Oncogene Proteins / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2
  • Rats
  • Signal Transduction
  • Staurosporine

Substances

  • Alkaloids
  • Growth Substances
  • Protein Synthesis Inhibitors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Staurosporine