YFH1-mediated iron homeostasis is independent of mitochondrial respiration

被引：10

作者：

Chen, OS ^{[1
]}

Kaplan, J ^{[1
]}

机构：

[1] Univ Utah, Sch Med, Dept Pathol, Salt Lake City, UT 84132 USA

来源：

FEBS LETTERS | 2001年 / 509卷 / 01期

关键词：

mitochondrial respiration; iron; yeast; YFH1; frataxin; Friedreich ataxia;

D O I：

10.1016/S0014-5793(01)03137-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The human gene frataxin and its yeast homolog YFH1 affect mitochondrial function. Deficits in frataxin result in Friedreich ataxia, while deletion of YFH1 results in respiratory incompetence. We determined that as long as respiratory incompetent yeast express Yfh1p they do not accumulate excessive mitochondrial iron. Deletion of YFH1 in respiratory incompetent yeast results in mitochondrial iron accumulation, while the reintroduction of Yfh1p results in mitochondrial iron export. Further, overexpression of Yfh1p has no effect on oxygen consumption in wild-type yeast grown in either fermentative or respiratory carbon sources. We conclude that the effect of Yfh1p on mitochondrial iron metabolism is independent of respiratory activity. (C) 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.

引用

页码：131 / 134

页数：4

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