Metabolism in the Caenorhabditis elegans Mit mutants

Abstract

In many eukaryotes oxidative phosphorylation via the mitochondrial electron transport chain provides the major means of ATP production. Complete removal of this capacity often results in premature death. Recent studies using the nematode Caenorhabditis elegans are surprising because they have revealed that disruption of many of the key components of the normal mitochondrial energy-generating machinery do not result in death, rather they result in adult life span extension. Such mutants have been collectively termed Mit mutants. In this short review, the potential use of alternate metabolic pathways for energy generation by Mit mutants will be considered. The effects of using such pathways on residual mitochondrial functionality, reactive radical species production, and longevity will also be explored.