Kaneko T, Watanabe T, Oishi M
Institute of Applied Microbiology, University of Tokyo, Japan.
Mol Cell Biol. 1988 Aug;8(8):3311-5. doi: 10.1128/mcb.8.8.3311-3315.1988.
When mouse erythroleukemia (MEL) cells were incubated in the presence of chloramphenicol (a specific inhibitor for mitochondrial protein synthesis) during the early stage of in vitro erythroid differentiation, the number of induced erythroid cells was greatly reduced. By use of cell fusion between two genetically marked MEL cells, this finding was further investigated. We found that the drug, along with other agents which inhibit mitochondrial protein synthesis, blocked the induction and turnover of the DMSO-inducible intracellular-erythroid-inducing activity (differentiation-inducing factor II) in a manner similar to that of cycloheximide, an inhibitor for nuclear protein synthesis. The inhibitory effect was confirmed by directly assaying differentiation-inducing factor II in the cell extracts. These results strongly suggest that mitochondrial protein synthesis is closely associated with in vitro erythroid differentiation of MEL cells.
当在体外红细胞分化早期将小鼠红白血病(MEL)细胞置于氯霉素(线粒体蛋白质合成的特异性抑制剂)存在的条件下培养时,诱导产生的红细胞数量大幅减少。通过对两个基因标记的MEL细胞进行细胞融合,对这一发现进行了进一步研究。我们发现,该药物与其他抑制线粒体蛋白质合成的试剂一起,以类似于环己酰亚胺(一种核蛋白质合成抑制剂)的方式,阻断了二甲基亚砜诱导的细胞内红细胞诱导活性(分化诱导因子II)的诱导和周转。通过直接检测细胞提取物中的分化诱导因子II,证实了这种抑制作用。这些结果有力地表明,线粒体蛋白质合成与MEL细胞的体外红细胞分化密切相关。