Department of Chemistry, Graduate School of Science, Nagoya University, and Chikusa-ku, Nagoya 464-8602, Japan.
Biochem Biophys Res Commun. 2010 Feb 5;392(2):228-33. doi: 10.1016/j.bbrc.2010.01.024. Epub 2010 Jan 13.
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 tam41Delta cells and partially restored the destabilized TIM23 complex structure in tam41Delta 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.
正常的线粒体蛋白导入需要线粒体外膜和内膜中的多个转位酶复合物。Tam41 是一种位于内膜周边的蛋白,参与内膜转位酶 TIM23 复合物的结构维持。在这里,我们鉴定出一种与 arrestin 相关的蛋白 Art5 是 Tam41 缺失酵母突变体的多拷贝抑制因子,该突变体表现出 TIM23 复合物的恶化和对温度敏感的生长缺陷。Art5 的过表达抑制了 tam41Delta 细胞的生长缺陷,并部分恢复了 tam41Delta 线粒体中不稳定的 TIM23 复合物结构,从而部分恢复了通过 TIM23 复合物进行的线粒体蛋白导入缺陷。反过来,ART5 基因的缺失与 TAM41 的缺失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 复合物方面的精确功能提供一个起点。