Identification of yeast Art5 as a multicopy suppressor for the mitochondrial translocator maintenance protein Tam41
Identification of yeast Art5 as a multicopy suppressor for the mitochondrial translocator maintenance protein Tam41
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DOI：
10.1016/j.bbrc.2010.01.024
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发表时间：
2010-02-05
影响因子：
3.1
通讯作者：
Endo, Toshiya
中科院分区：
文献类型：
--
作者：
Harada, Yoshihiro;Tamura, Yasushi;Endo, Toshiya
正常的线粒体蛋白输入需要线粒体内外膜的多个转运复合物。Tam41是外周内膜蛋白，参与内膜转运体TIM23复合体的结构维持。在这里，我们发现了一个抑制蛋白相关蛋白Art5作为tam41缺陷酵母突变体的多拷贝抑制因子，该突变体表现出恶化的TIM23复合体和温度敏感的生长缺陷。过表达Art5抑制了tam41 Delta细胞的生长缺陷，部分恢复了tam41 Delta线粒体中不稳定的TIM23复合体结构，从而部分恢复了通过TIM23复合体导入线粒体蛋白的缺陷。而在TAM41基因缺失的同时，ART5基因的缺失又表现出合成生长缺陷。Art5作为Tam41的功能伙伴，将为揭示Tam41在维持TIM23复合体中的精确功能提供一个起点。(C) 2010爱思唯尔公司所有航班预订。
Normal mitochondrial protein import requires multiple translocator complexes in the outer and inner mitochondrial membrane. Tam41 is a peripheral inner membrane protein that is involved in the structural maintenance of the inner membrane translocator the TIM23 complex. Here we identified an arrestin-related protein Art5 as a multicopy Suppressor for the Tam41-deficient yeast mutant, which exhibited the deteriorated TIM23 complex and temperature-sensitive growth defects. Overexpression of Art5 suppressed growth defects of tam41 Delta cells and partially restored the destabilized TIM23 complex structure in tam41 Delta mitochondria, so that the defects in mitochondrial protein import via the TIM23 complex were partially recovered. Deletion of the ART5 gene in turn exhibited synthetic growth defects with the TAM41 deletion. Art5 as a functional partner for Tam41 will provide a starting point to reveal the precise function of Tam41 in the maintenance of the TIM23 complex. (C) 2010 Elsevier Inc. All Fights reserved.