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Knock‐out of the cyaY gene in Escherichia coli does not affect cellular iron content and sensitivity to oxidants
Author(s) -
Li Dong Sheng,
Ohshima Keiichi,
Jiralerspong Sarn,
Bojanowski Michel W.,
Pandolfo Massimo
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)00896-0
Subject(s) - frataxin , escherichia coli , iron binding proteins , gene , biology , mitochondrion , bacteria , ataxia , oxidative stress , genetics , biochemistry , neuroscience
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 γ‐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 H 2 O 2 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.