Role of CED-4 in the activation of CED-3

Arul M. Chinnaiyan, Divya Chaudhary, Karen O'Rourke, Eugene V. Koonin and Vishva M. Dixit ()
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Arul M. Chinnaiyan: University of Michigan Medical School
Divya Chaudhary: University of Michigan Medical School
Karen O'Rourke: University of Michigan Medical School
Eugene V. Koonin: National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Building 38A
Vishva M. Dixit: Genentech, Inc., 1 DNA Way, M/S-40

Nature, 1997, vol. 388, issue 6644, 728-729

Abstract: Abstract Genetic analyses of the nematode Caenorhabditis elegans have identified three core components of the cell-death apparatus1. CED-3 and CED-4 promote, whereas CED-9 inhibits cell death. Recent studies indicate that CED-4 might interact independently with CED-3 and CED-9, forming the crux of a multicomponent death complex2. But except for its role as an adaptor molecule, little is known about CED-4 function. A clue came with the observation that mutation of the phosphate-binding loop (P-loop) of CED-4 disrupts its ability to induce chromatin condensation in yeast3. Further, a P-loop mutant of CED-4 (CED-4K165R) fails to process CED-3 in vivo, both in insect4 and mammalian cells (unpublished). We now confirm that CED-4 induces CED-3 activation and subsequent apoptosis, and that the process requires binding of ATP.

Date: 1997
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DOI: 10.1038/41913

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