Knock-out of the cyaY gene in Escherichia coli does not affect cellular iron content and sensitivity to oxidants

FEBS Lett. 1999 Jul 30;456(1):13-6. doi: 10.1016/s0014-5793(99)00896-0.


Friedreich ataxia is a recessively inherited neurodegenerative disease caused by deficiency of a highly conserved mitochondrial protein, frataxin. Frataxin deficiency results in mitochondrial iron accumulation and oxidative stress. Frataxin shows homology with the CyaY proteins of gamma-purple bacteria, whose function is unknown. We knocked out the CyaY gene in Escherichia coli MM383 by homologous recombination and we generated an E. coli MM383 strain overexpressing CyaY. Bacterial growth, iron content and survival after exposure to H2O2 did not differ among these strains, suggesting that, despite structural similarities, cyaY proteins in bacteria may have a different function from frataxin homologues in mitochondria.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amino Acid Sequence
  • Bacterial Proteins / drug effects
  • Bacterial Proteins / genetics*
  • Bacterial Proteins / metabolism*
  • Cell Division / genetics
  • Conserved Sequence
  • Escherichia coli / drug effects*
  • Escherichia coli / genetics*
  • Escherichia coli / metabolism
  • Escherichia coli Proteins
  • Gene Expression Regulation, Bacterial
  • Iron / metabolism*
  • Iron-Binding Proteins*
  • Mitochondria / metabolism
  • Molecular Sequence Data
  • Oxidants / pharmacology*
  • Oxidative Stress
  • Phosphotransferases (Alcohol Group Acceptor) / genetics
  • Recombination, Genetic


  • Bacterial Proteins
  • CyaY protein, E coli
  • Escherichia coli Proteins
  • Iron-Binding Proteins
  • Oxidants
  • frataxin
  • Iron
  • Phosphotransferases (Alcohol Group Acceptor)