Raff M C, Barres B A, Burne J F, Coles H S, Ishizaki Y, Jacobson M D
MRC Laboratory for Molecular Cell Biology, University College London, U.K.
Philos Trans R Soc Lond B Biol Sci. 1994 Aug 30;345(1313):265-8. doi: 10.1098/rstb.1994.0104.
We draw the following tentative conclusions from our studies on programmed cell death (PCD): (i) the amount of normal cell death in mammalian development is still underestimated; (ii) most mammalian cells constitutively express the proteins required to undergo PCD; (iii) the death programme operates by default when a mammalian cell is deprived of signals from other cells; (iv) many normal cell deaths may occur because cells fail to obtain the extracellular signals they need to suppress the death programme; and (v) neither the nucleus nor mitochondrial respiration is required for PCD (or Bcl-2 protection from PCD), raising the possibility that the death programme, like mitosis, is orchestrated by a cytosolic regulator that acts on multiple organelles in parallel.