Vest Katherine E, Wang Jing, Gammon Micah G, Maynard Margaret K, White Olivia L, Cobine Jai A, Mahone Wilkerson K, Cobine Paul A
Department of Biological Sciences, Auburn University, Auburn, AL 36849, USA.
College of Charleston, Charleston, SC 29424, USA.
Open Biol. 2016 Jan;6(1):150223. doi: 10.1098/rsob.150223.
In Saccharomyces cerevisiae, the mitochondrial carrier family protein Pic2 imports copper into the matrix. Deletion of PIC2 causes defects in mitochondrial copper uptake and copper-dependent growth phenotypes owing to decreased cytochrome c oxidase activity. However, copper import is not completely eliminated in this mutant, so alternative transport systems must exist. Deletion of MRS3, a component of the iron import machinery, also causes a copper-dependent growth defect on non-fermentable carbon. Deletion of both PIC2 and MRS3 led to a more severe respiratory growth defect than either individual mutant. In addition, MRS3 expressed from a high copy number vector was able to suppress the oxygen consumption and copper uptake defects of a strain lacking PIC2. When expressed in Lactococcus lactis, Mrs3 mediated copper and iron import. Finally, a PIC2 and MRS3 double mutant prevented the copper-dependent activation of a heterologously expressed copper sensor in the mitochondrial intermembrane space. Taken together, these data support a role for the iron transporter Mrs3 in copper import into the mitochondrial matrix.
在酿酒酵母中，线粒体载体家族蛋白Pic2将铜导入线粒体基质。PIC2基因的缺失会导致线粒体铜摄取缺陷以及由于细胞色素c氧化酶活性降低而出现铜依赖性生长表型。然而，在该突变体中铜的导入并未完全消除，因此必定存在其他转运系统。铁导入机制的组成部分MRS3基因的缺失，也会导致在非发酵碳源上出现铜依赖性生长缺陷。PIC2和MRS3基因均缺失导致的呼吸生长缺陷比单个突变体更为严重。此外，从高拷贝数载体表达的MRS3能够抑制缺乏PIC2的菌株的氧气消耗和铜摄取缺陷。当在乳酸乳球菌中表达时，Mrs3介导铜和铁的导入。最后，PIC2和MRS3双突变体阻止了线粒体膜间隙中异源表达的铜传感器的铜依赖性激活。综上所述，这些数据支持铁转运蛋白Mrs3在将铜导入线粒体基质中发挥作用。
