Yaffe M P, Schatz G
Proc Natl Acad Sci U S A. 1984 Aug;81(15):4819-23. doi: 10.1073/pnas.81.15.4819.
We isolated two yeast mutants that are temperature-sensitive for import of mitochondrial proteins. Each strain contains a single mutation that results in arrest of growth and accumulation of precursor to the beta subunit of the mitochondrial F1-ATPase after incubation at 37 degrees C. These lesions (mas1 and mas2) are nonallelic and recessive. Cells harboring either mutation stop growing only after 2-3 generations at 37 degrees C. Import of the F1 beta subunit at 37 degrees C is more than 250 times slower in mas1 and 15 times slower in mas2 than in wild-type cells. At 23 degrees C, import occurs with similar rates in mutant and wild-type cells. The two mutations also reduce the rate of import of other proteins; however, import of different precursors is affected to different degrees in the two strains. The temperature-sensitive step in import in both mas1 and mas2 occurs before arrival of precursors in the mitochondrial matrix.
我们分离出了两个对线粒体蛋白导入具有温度敏感性的酵母突变体。每个菌株都含有一个单一突变,该突变导致在37℃孵育后,线粒体F1 - ATP酶β亚基的前体积累且生长停滞。这些损伤(mas1和mas2)是非等位基因且隐性的。携带任一突变的细胞在37℃下仅经过2 - 3代就停止生长。在37℃时,mas1中F1β亚基的导入速度比野生型细胞慢250倍以上,mas2中慢15倍。在23℃时,突变体和野生型细胞中导入的速率相似。这两个突变也降低了其他蛋白质的导入速率;然而,不同前体的导入在这两个菌株中受到的影响程度不同。mas1和mas2中导入的温度敏感步骤发生在前体到达线粒体基质之前。