Knock-out of the cyaY gene in Escherichia coli does not affect cellular iron content and sensitivity to oxidants
Knock-out of the cyaY gene in Escherichia coli does not affect cellular iron content and sensitivity to oxidants
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DOI：
10.1016/s0014-5793(99)00896-0
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发表时间：
1999-07-30
期刊：
影响因子：
3.5
通讯作者：
Pandolfo, M
中科院分区：
文献类型：
--
作者：
Li, DS;Ohshima, K;Pandolfo, M
Friedreich 共济失调是一种隐性遗传的神经退行性疾病，由高度保守的线粒体蛋白 frataxin 缺乏引起，frataxin 缺乏会导致线粒体铁积累和氧化应激。 Frataxin 与γ-紫细菌的 CyaY 蛋白具有同源性，但其功能尚不清楚。我们通过同源重组敲除大肠杆菌 MM383 中的 CyaY 基因，并生成过表达 CyaY 的大肠杆菌 MM383 菌株。这些菌株在暴露于 H2O2 后的细菌生长、铁含量和存活率没有差异，这表明，尽管结构相似，细菌中的 cyaY 蛋白可能与线粒体中的 frataxin 同源物具有不同的功能，(C) 1999 年欧洲联合会生化学会。
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, (C) 1999 Federation of European Biochemical Societies.