Journal
SCIENCE
Volume 328, Issue 5976, Pages 327-334Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1182374
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Funding
- Burroughs Wellcome Fund Award
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan
- NIH [R01 GM59083, R01 GM79097]
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Chromosome fragmentation is a hallmark of apoptosis, conserved in diverse organisms. In mammals, caspases activate apoptotic chromosome fragmentation by cleaving and inactivating an apoptotic nuclease inhibitor. We report that inactivation of the Caenorhabditis elegans dcr-1 gene, which encodes the Dicer ribonuclease important for processing of small RNAs, compromises apoptosis and blocks apoptotic chromosome fragmentation. DCR-1 was cleaved by the CED-3 caspase to generate a C-terminal fragment with deoxyribonuclease activity, which produced 3' hydroxyl DNA breaks on chromosomes and promoted apoptosis. Thus, caspase-mediated activation of apoptotic DNA degradation is conserved. DCR-1 functions in fragmenting chromosomal DNA during apoptosis, in addition to processing of small RNAs, and undergoes a protease-mediated conversion from a ribonuclease to a deoxyribonuclease.
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