Heude M, Chanet R
Mutat Res. 1975 Apr;28(1):47-55. doi: 10.1016/0027-5107(75)90313-9.
The contribution of mitochondrial proteins in the repair of UV-induced lethal and cytoplasmic genetic damages was studied in dark liquid held exponential and stationary phase yeast cells. This was performed by using the specific inhibitors, erythromycin (ER) anc chloramphenicol (CAP). It was shown that mitochondrial proteins are involved in the recovery of stationary phase cells. Mitochondrial proteins are partly implicated in the mechanisms leading to the restoration of the (see article) genotype in UV-irradiated dark liquid held exponential phase cells. Here again, in stationary phase cells, mitochondrial enzymes do not seem to participate in the negative liquid holding (NLH) process for the (see article) induction, as shown by inhibiting mitochondrial protein synthesis or both mitochondrial and nuclear protein synthesis. When cells are grown in glycerol, the response after dark liquid holding of UV-treated cells in the different growth stages are similar to that found for glucose-grown cells. In other words, the fate of cytoplasmic genetic damage, in particular, is not correlated with the repressed or derepressed state of the mitochondria.
在处于指数生长期和稳定期的黑暗液体培养酵母细胞中,研究了线粒体蛋白在修复紫外线诱导的致死性和细胞质遗传损伤中的作用。这是通过使用特异性抑制剂红霉素(ER)和氯霉素(CAP)来进行的。结果表明,线粒体蛋白参与稳定期细胞的恢复过程。线粒体蛋白部分参与了导致紫外线照射的黑暗液体培养指数期细胞(见文章)基因型恢复的机制。同样,在稳定期细胞中,如通过抑制线粒体蛋白合成或线粒体和核蛋白合成,线粒体酶似乎不参与(见文章)诱导的负液体培养(NLH)过程。当细胞在甘油中生长时,不同生长阶段紫外线处理细胞黑暗液体培养后的反应与葡萄糖培养细胞相似。换句话说,特别是细胞质遗传损伤的命运与线粒体的抑制或去抑制状态无关。