Posttranslational Regulation of the Scaffold for Fe-S Cluster Biogenesis, Isu
Posttranslational Regulation of the Scaffold for Fe-S Cluster Biogenesis, Isu
复制标题
DOI：
10.1091/mbc.e08-06-0622
复制
发表时间：
2008-12-01
影响因子：
3.3
通讯作者：
Craig, Elizabeth A.
中科院分区：
文献类型：
--
作者：
Andrew, Amy J.;Song, Ji-Yoon;Craig, Elizabeth A.
Isu是Fe-S簇在线粒体基质中构建的支架蛋白，在Fe-S簇蛋白的生物发生中起着核心作用。我们报告说，在集群生物发生系统，包括专门的Hsp 70 Ssq 1的几个组件的活动减少，导致15-20倍上调的Isu。这种上调是由转录和翻译后水平的变化引起的：ISU mRNA水平的增加和ISU蛋白的稳定性。它的生物学重要性通过以下事实证明：当Isu水平被阻止上升到野生型细胞中发现的水平时，缺乏Ssq 1的细胞生长不良。在所测试的生物成因因子中，硫供体Nfs 1是唯一的。当Nfs 1耗尽时，Isu水平几乎没有增加。然而，它的存在是由其他组分的活性降低引起的上调所必需的。我们的研究结果是一致的存在的机制，以增加的稳定性Isu，从而其水平，这是依赖于半胱氨酸脱硫酶Nfs 1的存在。
Isu, the scaffold protein on which Fe-S clusters are built in the mitochondrial matrix, plays a central role in the biogenesis of Fe-S cluster proteins. We report that the reduction in the activity of several components of the cluster biogenesis system, including the specialized Hsp70 Ssq1, causes a 15-20-fold up-regulation of Isu. This up-regulation results from changes at both the transcriptional and posttranslational level: an increase in ISU mRNA levels and in stability of ISU protein. Its biological importance is demonstrated by the fact that cells lacking Ssq1 grow poorly when Isu levels are prevented from rising above those found in wild-type cells. Of the biogenesis factors tested, Nfs1, the sulfur donor, was unique. Little increase in Isu levels occurred when Nfs1 was depleted. However, its presence was required for the up-regulation caused by reduction in activity of other components. Our results are consistent with the existence of a mechanism to increase the stability of Isu, and thus its level, that is dependent on the presence of the cysteine desulfurase Nfs1.