Metabolism in the Caenorhabditis elegans Mit mutants.
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.
Rea
Shane L
SL
Institute for Behavioral Genetics, University of Colorado, Campus Box 447, Boulder, CO 80309-0447, USA. srea@colorado.edu
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000378:metabolism*; D045222:Electron Transport Chain Complex Proteins / Q000235:genetics*; D004734:Energy Metabolism / Q000235:genetics; D005993:Glycerolphosphate Dehydrogenase / Q000378:metabolism; D015801:Helminth Proteins / Q000235:genetics / Q000378:metabolism; D008136:Longevity / Q000235:genetics*; D008928:Mitochondria / Q000378:metabolism*; D009154:Mutation; D017382:Reactive Oxygen Species / Q000378:metabolism
D045222:Electron Transport Chain Complex Proteins; D015801:Helminth Proteins; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D005993:Glycerolphosphate Dehydrogenase