Programmed cell death and Bcl‐2 protection in the absence of a nucleus.

It is shown that anucleate cytoplasts can undergo programmed cell death 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 B cl‐2 or survival factor protection.

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.