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

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 Lett

journal_title

FEBS letters

authors

Li DS,Ohshima K,Jiralerspong S,Bojanowski MW,Pandolfo M

doi

10.1016/s0014-5793(99)00896-0

keywords:

subject

Has Abstract

pub_date

1999-07-30 00:00:00

pages

13-6

issue

1

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(99)00896-0

journal_volume

456

pub_type

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