Suppression of CED-3-independent apoptosis by mitochondrial βNAC in Caenorhabditis elegans

Tim A. Bloss, Eric S. Witze and Joel H. Rothman ()
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Tim A. Bloss: University of California
Eric S. Witze: University of California
Joel H. Rothman: University of California

Nature, 2003, vol. 424, issue 6952, 1066-1071

Abstract: Abstract To ensure cell survival, it is essential that the ubiquitous pro-apoptotic machinery is kept quiescent. As death is irreversible, cells must continually integrate developmental information with regulatory inputs to control the switch between repressing and activating apoptosis. Inappropriate activation or suppression of apoptosis can lead to degenerative pathologies1 or tumorigenesis2, respectively. Here we report that Caenorhabditis elegans inhibitor of cell death-1 (ICD-1) is necessary and sufficient to prevent apoptosis. Loss of ICD-1 leads to inappropriate apoptosis in developing and differentiated cells in various tissues. Although this apoptosis requires CED-4, it occurs independently of CED-3—the caspase essential for developmental apoptosis3—showing that these core pro-apoptotic proteins have separable roles. Overexpressing ICD-1 inhibits the apoptosis of cells that are normally programmed to die. ICD-1 is the β-subunit of the nascent polypeptide-associated complex (βNAC) and contains a putative caspase-cleavage site and caspase recruitment domain. It localizes primarily to mitochondria, underscoring the role of mitochondria in coordinating apoptosis4. Human βNAC is a caspase substrate that is rapidly eliminated in dying cells5,6, suggesting that ICD-1 apoptosis-suppressing activity may be inactivated by caspases.

Date: 2003
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DOI: 10.1038/nature01920

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