Abstract:
: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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Li DS,Ohshima K,Jiralerspong S,Bojanowski MW,Pandolfo Mdoi
10.1016/s0014-5793(99)00896-0keywords:
subject
Has Abstractpub_date
1999-07-30 00:00:00pages
13-6issue
1eissn
0014-5793issn
1873-3468pii
S0014-5793(99)00896-0journal_volume
456pub_type
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