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

FEBS Letters

Pandolfo, Massimo¹  Jiralerspong, Sarn¹  Ohshima, Keiichi¹  Bojanowski, Michel W.²  Li, Dong Sheng¹ 

[1] Research Center, Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, 1560 rue Sherbrooke est, Montreal, Que. H2L 4M1, Canada;Service of Neurosurgery, Centre Hospitalier de l'Université de Montréal, Hôpital Notre-Dame, 1560 rue Sherbrooke est, Montreal, Que. H2L 4M1, Canada

关键词: Friedreich ataxia;    CyaY;    Iron;    Free radical;    Hydrogen peroxide;    Escherichia coli;   

DOI  :  10.1016/S0014-5793(99)00896-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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 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.

【 授权许可】

Unknown