Mitochondrial endonuclease G is important for apoptosis in C. elegans

Jay Parrish, Lily Li, Kristina Klotz, Duncan Ledwich, Xiaodong Wang and Ding Xue ()
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Jay Parrish: Cellular, and Developmental Biology, University of Colorado
Lily Li: University of Texas Southwestern Medical Center
Kristina Klotz: Cellular, and Developmental Biology, University of Colorado
Duncan Ledwich: Cellular, and Developmental Biology, University of Colorado
Xiaodong Wang: University of Texas Southwestern Medical Center
Ding Xue: Cellular, and Developmental Biology, University of Colorado

Nature, 2001, vol. 412, issue 6842, 90-94

Abstract: Abstract Programmed cell death (apoptosis) is a tightly regulated process of cell disassembly in which dying cells and their nuclei shrink and fragment and the chromosomal DNA is degraded into internucleosomal repeats1,2,3. Here we report the characterization of the cps-6 gene, which appears to function downstream of, or in parallel to, the cell-death protease CED-3 of Caenorhabditis elegans in the DNA degradation process during apoptosis. cps-6 encodes a homologue of human mitochondrial endonuclease G4,5, and its protein product similarly localizes to mitochondria in C. elegans. Reduction of cps-6 activity caused by a genetic mutation or RNA-mediated interference (RNAi) affects normal DNA degradation, as revealed by increased staining in a TUNEL assay, and results in delayed appearance of cell corpses during development in C. elegans. This observation provides in vivo evidence that the DNA degradation process is important for proper progression of apoptosis. CPS-6 is the first mitochondrial protein identified to be involved in programmed cell death in C. elegans, underscoring the conserved and important role of mitochondria in the execution of apoptosis.

Date: 2001
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DOI: 10.1038/35083608

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