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

Friedreich ataxia is a recessively inherited neurodegenerative disease caus ed by deficiency of a highly conserved mitochondrial protein, frataxin, Fra taxin deficiency results in mitochondrial iron accumulation and oxidative s tress. Frataxin shows homology with the CyaY proteins of gamma-purple bacte ria, whose function is unknown. We knocked out the CyaY gene in Escherichia coli MM383 by homologous recombination and we generated an E. coli MM383 s train overexpressing CyaY, Bacterial growth, iron content and survival afte r exposure to H2O2 did not differ among these strains, suggesting that, des pite structural similarities, cyaY proteins in bacteria may have a differen t function from frataxin homologues in mitochondria, (C) 1999 Federation of European Biochemical Societies.