Mitochondrial electron transport is a key determinant of life span in Caenorhabditis elegans

Dev Cell. 2001 Nov;1(5):633-44. doi: 10.1016/s1534-5807(01)00071-5.

Abstract

Increased protection from reactive oxygen species (ROS) is believed to increase life span. However, it has not been clearly demonstrated that endogenous ROS production actually limits normal life span. We have identified a mutation in the Caenorhabditis elegans iron sulfur protein (isp-1) of mitochondrial complex III, which results in low oxygen consumption, decreased sensitivity to ROS, and increased life span. Furthermore, combining isp-1(qm150) with a mutation (daf-2) that increases resistance to ROS does not result in any significant further increase in adult life span. These findings indicate that both isp-1 and daf-2 mutations increase life span by lowering oxidative stress and result in the maximum life span increase that can be produced in this way.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Caenorhabditis elegans / embryology
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans / growth & development
  • Caenorhabditis elegans / metabolism*
  • Caenorhabditis elegans Proteins / chemistry
  • Caenorhabditis elegans Proteins / genetics
  • Caenorhabditis elegans Proteins / metabolism
  • Cloning, Molecular
  • Cytochrome b Group / genetics
  • Cytochrome b Group / metabolism
  • Electron Transport / drug effects
  • Electron Transport / genetics
  • Electron Transport Complex III / chemistry
  • Electron Transport Complex III / genetics
  • Electron Transport Complex III / metabolism*
  • Forkhead Transcription Factors
  • Helminth Proteins / genetics
  • Humans
  • Iron-Sulfur Proteins / chemistry
  • Iron-Sulfur Proteins / genetics
  • Iron-Sulfur Proteins / metabolism*
  • Longevity* / genetics
  • Mitochondria / chemistry
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • Models, Molecular
  • Mutation
  • Oxidative Stress* / drug effects
  • Oxidative Stress* / genetics
  • Oxygen / metabolism
  • Oxygen Consumption / drug effects
  • Oxygen Consumption / genetics
  • Paraquat / pharmacology
  • Phenotype
  • Protein Conformation
  • Reactive Oxygen Species / metabolism
  • Receptor, Insulin / genetics
  • Receptor, Insulin / metabolism
  • Sequence Homology, Amino Acid
  • Transcription Factors / genetics
  • Transcription Factors / metabolism

Substances

  • CLK-1 protein, C elegans
  • Caenorhabditis elegans Proteins
  • Cytochrome b Group
  • Forkhead Transcription Factors
  • Helminth Proteins
  • Iron-Sulfur Proteins
  • Reactive Oxygen Species
  • Transcription Factors
  • daf-16 protein, C elegans
  • Isp-1 protein, Caenorhabditis elegans
  • DAF-2 protein, C elegans
  • Receptor, Insulin
  • Electron Transport Complex III
  • Paraquat
  • Oxygen