In 1997, to the surprise of many researchers, mitochondria reclaimed the limelight of apoptosis research when several groups observed that cytochrome c released from the mitochondria could induce apoptosis in cell-free systems.1,2 A hot research topic decades ago, mitochondria excitement cooled in the 1970s when researchers agreed on the mechanisms of oxidative phosphorylation (ox-phos). Now, mitochondria-mediated apoptosis is believed to be central to a number of major debilitating diseases, including Parkinson's disease and cancer.3,4
Just why mitochondria assume this seemingly disparate role is the subject of speculation. Neil Blackstone, associate professor of biological sciences, Northern Illinois University, DeKalb, and Douglas Green, head of the division of immunology at the La Jolla Institute for Allergy and Immunology, Ontario, Calif., believe that it is an evolutionary issue, one that goes back to the mitochondria's roots as an endosymbiont.5 They suggest that after ancient eukaryotes took in protomitochondria, mitochondria...
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