Brux B, Herrmann D, Richter G, Fleck W F, Strauss D G, Koch W
Nucleic Acids Res. 1981 Feb 25;9(4):1005-18. doi: 10.1093/nar/9.4.1005.
The effect of three components of the anthracycline antibiotic violamycin on the transcription of bacteriophage T3 DNA by bacteriophage T3-induced RNA polymerase has been investigated in a cell-free system. The glycosides of violamycin BI possess the highest inhibitory activity, whereas those of violamycin BII and violamycin A show a reduced inhibitory effect. Concentrations of violamycin BI depressing the incorporation of (3H)UMP into RNA chains have only a slight effect on the binding of the T3 RNA polymerase to T3 DNA and on the incorporation of GTP as the first nucleotide. This shows that the primary target of the antibiotic is not the initiation of the RNA synthesis. The binding of violamycin BI to T3 DNA causes a strong reduction of the elongation rate of the RNA chains.
在无细胞体系中研究了蒽环类抗生素紫霉素的三种组分对噬菌体T3诱导的RNA聚合酶转录噬菌体T3 DNA的影响。紫霉素BI的糖苷具有最高的抑制活性,而紫霉素BII和紫霉素A的糖苷抑制作用减弱。抑制(3H)UMP掺入RNA链的紫霉素BI浓度对T3 RNA聚合酶与T3 DNA的结合以及作为第一个核苷酸的GTP掺入仅有轻微影响。这表明该抗生素的主要作用靶点不是RNA合成的起始。紫霉素BI与T3 DNA的结合导致RNA链延伸速率大幅降低。