Scission, spores, and apoptosis: a proposal for the evolutionary origin of mitochondria in cell death induction.
Mitochondria fragment prior to caspase activation during many pathways of apoptosis. Inhibition of the machinery that normally regulates mitochondrial morphology in healthy cells inhibits the fission that occurs during apoptosis and actually delays the process of cell death. Interestingly, there are certain parallels between mitochondrial fission and bacterial sporulation. As bacterial sporulation can be considered a stress response we suggest that a primordial stress response of endosymbiont mitochondrial progenitors may have been adopted for the stress response of early eukaryotes. Thus, the mitochondrial fission process may represent an early stress response of primitive mitochondria that could have integrated the stress signals and acted as an initial sensor for the eukaryotic response system. The fact that mitochondria fragment during apoptosis using the machinery descended from or that superceded the bacterial stress response of sporulation is consistent with this hypothesis. This hypothesis would explain why what is generally considered the "power house" of the cell came to integrate the cell death response and regulate apoptosis.
Biochemistry Section, SNB, NINDS/NIH, Building 10, Room 5D-37, Bethesda, MD 20892, USA.
Stephan
S
Frank
Everett G
EG
Robert
Richard J
RJ
Youle
D017209:Apoptosis; D001419:Bacteria / Q000648:ultrastructure; D018407:Bacterial Physiological Phenomena; D001426:Bacterial Proteins / Q000378:metabolism; D005075:Biological Evolution; D016923:Cell Death; D003598:Cytoskeletal Proteins; D008928:Mitochondria / Q000145:classification / Q000502:physiology* / Q000648:ultrastructure; D008954:Models, Biological; D010802:Phylogeny; D013171:Spores, Bacterial / Q000648:ultrastructure
D001426:Bacterial Proteins; D003598:Cytoskeletal Proteins; C071525:FtsZ protein, Bacteria