Cocito C, Vanlinden F, Branlant C
Biochim Biophys Acta. 1983 Mar 10;739(2):158-63. doi: 10.1016/0167-4781(83)90025-8.
The M component of virginiamycin blocks protein synthesis by inactivating catalytically the 50 S ribosomal subunits: the in vitro interaction of 50 S with virginiamycin M, followed by removal of the antibiotic, results in a lasting damage of the particle. This enzyme-like inactivation of 50 S subunits resembles that of 30 S subunits by colicin E3, which entails the cleavage of 16 S rRNA. To explore this possibility, rRNA obtained from particles incubated in vivo and in vitro with virginiamycin M were analyzed. Electrophoretic analysis of 5, 16 and 23 S rRNA did not reveal major changes, nor did it show the appearance of additional fragments. To exclude the possibility of terminal alterations, the 5'- and 3'-extremities of these RNA were also sequenced and found unchanged. Conclusions drawn in the present work parallel those of an accompanying paper (Moureau, P., Di Giambattista, M. and Cocito, C. (1983) Biochim. Biophys. Acta 739, 164-172) describing the dissociation and reassociation of ribosomes incubated with virginiamycin M: the lasting ribosome damage by this antibiotic appears to be due to a conformational rather than to a structural alteration.
维吉尼亚霉素的M组分通过催化失活50 S核糖体亚基来阻断蛋白质合成：50 S与维吉尼亚霉素M在体外相互作用，随后去除抗生素，会导致核糖体颗粒的永久性损伤。50 S亚基的这种类似酶的失活类似于大肠杆菌素E3对30 S亚基的失活，后者会导致16 S rRNA的切割。为了探究这种可能性，对在体内和体外与维吉尼亚霉素M一起孵育的核糖体颗粒所获得的rRNA进行了分析。对5、16和23 S rRNA的电泳分析未发现主要变化，也未显示出额外片段的出现。为了排除末端改变的可能性，还对这些RNA的5'和3'末端进行了测序，结果发现没有变化。本研究得出的结论与同期发表的一篇论文（Moureau, P., Di Giambattista, M.和Cocito, C. (1983) Biochim. Biophys. Acta 739, 164 - 172）的结论一致，该论文描述了与维吉尼亚霉素M一起孵育的核糖体的解离和重新结合：这种抗生素对核糖体的永久性损伤似乎是由于构象改变而非结构改变。
