Mitochondrial and cytoplasmic thioredoxin reductase variants encoded by a single Drosophila gene are both essential for viability

J Biol Chem. 2002 Mar 29;277(13):11521-6. doi: 10.1074/jbc.M111692200. Epub 2002 Jan 16.

Abstract

Defense against oxidative stress in mammals includes the regeneration of the major thiol reductants glutathione and thioredoxin by glutathione reductase and thioredoxin reductase (TrxR), respectively. In contrast, Drosophila, and possibly insects in general, lacks glutathione reductase and must rely solely on the TrxR system. The mammalian TrxRs described so far are selenoproteins that utilize NADPH to reduce protein as well as nonprotein substrates in mitochondria and cytoplasm of cells. We show that a single Drosophila gene, Trxr-1, encodes non-selenocysteine-containing cytoplasmic and mitochondrial TrxR isoforms that differ with respect to their N termini. We generated transcript-specific mutants and used in vivo approaches to explore the biological functions of the two enzyme variants by introducing the corresponding transgenes into different Trxr-1 mutants. The results show that, although the two TrxR isoforms have similar biochemical properties, their biological functions are not interchangeable.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cytoplasm / enzymology*
  • DNA Primers
  • Drosophila / enzymology
  • Drosophila / genetics*
  • Kinetics
  • Longevity / genetics
  • Mitochondria / enzymology*
  • Mutation
  • Oxidative Stress
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Thioredoxin-Disulfide Reductase / genetics*
  • Thioredoxin-Disulfide Reductase / metabolism

Substances

  • DNA Primers
  • Recombinant Proteins
  • Thioredoxin-Disulfide Reductase