Kuwano M, Matsui K, Takenaka K, Akiyama S, Endo H
Int J Cancer. 1977 Aug 15;20(2):296-302. doi: 10.1002/ijc.2910200219.
After nitrosoguanidine mutagenesis we isolated from mouse leukemia L5178Y cells a mutant cell (Bla-R) resistant to blasticidin S, an inhibitor of protein synthesis. Neither growth nor leucine incorporation into hot-acid insoluble fraction of Bla-R cell was inhibited by 5 to 20 microgram/ml blasticidin S, which almost completely blocked protein synthesis as well as growth of the parental L5178Y cells. However, other inhibitors such as fusidic acid, cycloheximide, ricin D or L-asparaginase blocked protein synthesis in Bla-R cells to the same extent as in L5178Y cells. Protein synthesis in vitro using S-30 extracts from the parental cell line L5178Y was almost completely blocked in the presence of the antibiotic, while no inhibition by blasticidin S occurred when S-30 extracts -rom Bla-R mutant cells were used. Protein synthesis assays were made by using the S100 fraction from rat liver together with ribosomes from either L5178Y cells or Bla-R cells. Blasticidin S inhibited protein synthesis when ribosomes were derived from L5178Y cells, but not from Bla-R mutant.
经亚硝基胍诱变后,我们从小鼠白血病L5178Y细胞中分离出一种对蛋白质合成抑制剂杀稻瘟菌素S具有抗性的突变细胞(Bla-R)。5至20微克/毫升的杀稻瘟菌素S对Bla-R细胞的生长和亮氨酸掺入热酸不溶性部分均无抑制作用,而该浓度的杀稻瘟菌素S几乎完全阻断了亲本L5178Y细胞的蛋白质合成及生长。然而,其他抑制剂如夫西地酸、环己酰亚胺、蓖麻毒素D或L-天冬酰胺酶对Bla-R细胞蛋白质合成的阻断程度与对L5178Y细胞的相同。在抗生素存在的情况下,使用亲本细胞系L5178Y的S-30提取物进行的体外蛋白质合成几乎完全被阻断,而使用Bla-R突变细胞的S-30提取物时,杀稻瘟菌素S未产生抑制作用。通过使用来自大鼠肝脏的S100部分以及来自L5178Y细胞或Bla-R细胞的核糖体进行蛋白质合成测定。当核糖体来自L5178Y细胞时,杀稻瘟菌素S抑制蛋白质合成,但来自Bla-R突变体时则不然。