Programmed cell death and Bcl-2 protection in the absence of a nucleus.
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.
Jacobson
M D
MD
Developmental Neurobiology Programme, MRC Laboratory for Molecular Cell Biology, London, UK.
Burne
J F
JF
Raff
M C
MC
D000470:Alkaloids / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology*; D002467:Cell Nucleus / Q000502:physiology*; D003593:Cytoplasm / Q000502:physiology*; D005347:Fibroblasts / Q000187:drug effects / Q000502:physiology; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D008954:Models, Biological; D009836:Oligodendroglia / Q000187:drug effects / Q000502:physiology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011518:Proto-Oncogene Proteins / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D015398:Signal Transduction; D019311:Staurosporine
D000470:Alkaloids; D006133:Growth Substances; D011500:Protein Synthesis Inhibitors; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D019311:Staurosporine