Mitochondria and apoptosis

Programmed cell death serves as a major mechanism for the precise regulation of cell numbers and as a defense mechanism to remove unwanted and potentially dangerous cells. Despite the striking heterogeneity of cell death induction pathways, the execution of the death program is often associated with characteristic morphological and biochemical changes, and this form of programmed cell death has been termed apoptosis.Genetic studies in Caenorhabditis elegans had led to the identification of cell death genes (ced). The genes ced‐3 and ced‐4 are essential for cell death; ced‐9 antagonizes the activities of ced‐3 and ced‐4, and thereby protects cells that should survive from any accidental activation of the death program. Caspases (cysteine aspartases) are the mammalian homologues of CED‐3. CED‐9 protein is homologous to a family of many members termed the Bcl‐2 family (Bcl‐2s) in reference to the first discovered mammalian cell death regulator. In both worm and mammalian cells, the antiapoptotic members of the Bcl‐2 family act upstream of the execution caspases somehow preventing their proteolytic processing into active killers.Two main mechanisms of action have been proposed to conne