Transcription of the yeast iron regulon does not respond directly to iron but rather to iron-sulfur cluster biosynthesis
Transcription of the yeast iron regulon does not respond directly to iron but rather to iron-sulfur cluster biosynthesis
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DOI：
10.1074/jbc.m403209200
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发表时间：
2004-07-09
影响因子：
4.8
通讯作者：
Kaplan, J
中科院分区：
文献类型：
--
作者：
Chen, OS;Crisp, RJ;Kaplan, J
酿酒酵母通过增加铁调节子的转录来响应铁剥夺，包括由FET 3和FTR 1编码的高亲和力细胞表面转运系统。在这里，我们表明，这些基因的转录不直接响应于胞质铁，而是铁的线粒体利用铁的铁硫（Fe-S）簇的合成。我们利用了一种突变形式的铁依赖性酶的固醇途径（Erg 25 - 2 p），以评估胞浆铁水平。我们发现，线粒体Fe-S生物合成的中断，导致线粒体铁积累过多，导致转录的铁转运系统独立的胞浆铁水平。线粒体含铁硫酶乌头酸酶的活性与FET 3的诱导之间存在负相关性。通过Fe-S生物合成调节转录代表细胞铁获取与线粒体铁代谢整合的机制。
Saccharomyces cerevisiae responds to iron deprivation by increased transcription of the iron regulon, including the high affinity cell-surface transport system encoded by FET3 and FTR1. Here we demonstrate that transcription of these genes does not respond directly to cytosolic iron but rather to the mitochondrial utilization of iron for the synthesis of iron-sulfur (Fe-S) clusters. We took advantage of a mutant form of an iron-dependent enzyme in the sterol pathway (Erg25-2p) to assess cytosolic iron levels. We showed that disruption of mitochondrial Fe-S biosynthesis, which results in excessive mitochondrial iron accumulation, leads to transcription of the iron transport system independent of the cytosolic iron level. There is an inverse correlation between the activity of the mitochondrial Fe-S-containing enzyme aconitase and the induction of FET3. Regulation of transcription by Fe-S biosynthesis represents a mechanism by which cellular iron acquisition is integrated with mitochondrial iron metabolism.