Programmed cell death throughout life influences the longevity of a defective mitochondrial mutant in C. elegans.

Abstract

In C. elegans , the mev-1 gene mutation leads to increased mitochondrial dysfunction and embryonic abnormal apoptosis, thereby shortening the lifespan. A mutation in the ced-3 gene encoding an ortholog of mammalian caspases reduces the excessive embryonic apoptosis and recovers the lifespan of the mev-1 mutant. Here, we report the difference between temporary in early development and continuous knockdowns of the ced-3 gene. We found that CED-3 /caspase is essential to the abnormal apoptosis in the mev-1 mutant, not only during development but also during aging. These findings indicate an association of CED-3 /caspase with age-related cellular dysfunction even in somatic cells.