Depression of Lethal Activity of Plasmid in Streptomycetes

我们发现，一些azureus链霉菌（Streptomyces azureus ATCC 14921）的衍生菌株由于其原始序列被整合到野生型菌株的染色体上的接合质粒pSA1.1的作用而失去了孢子形成能力和硫链菌的产率。pSA1.1与pSA1.1衍生的缺陷质粒pSA1.2共存，抑制了pSA1.1对孢子形成和硫链霉素产生的抑制能力。半胱氨酸和含半胱氨酸的化合物。杆菌肽和谷胱甘肽等也抑制了pSA1.1的抑制作用。这些化合物还能促进野生型和质粒固化菌株的孢子形成、空中菌丝伸长或Thiostrepton的产生：半胱氨酸表现出孢子形成活性、空中菌丝伸长弱活性和Thiostrepton的产生；杆菌肽在水中菌丝上表现出孢子形成活性和较强的生长活性，在地上菌丝上表现出较强的伸长活性；谷胱甘肽表现出孢子形成活性。这些化合物会促进细胞的新陈代谢。pSA1.1对宿主细胞的抑制作用可能因宿主细胞代谢增强而减弱。pSA1.1可能编码一种蛋白质，这种蛋白质可以与细胞膜以破坏方式相互作用。

We found that some derivatives of Streptomyces azureus ATCC 14921 lost both spore forming ability and Thiostrepton productivity due to the action of a conjugative plasmid pSA1.1, of which original sequence was integrated in the chromosome of wild-type strain. The inhibiting ability of pSA1.1 on the spore formation and Thiostrepton production was depressed by coexistence with a defective plasmid pSA1.2 derived from pSA1.1. Cysteine and cysteine-containing compounds.Such as Bacitracin and Glutathione also depressed the inhibiting action of pSA1.1. These compounds also stimulated the spore formation, aerial mycelium elongation or Thistrepton production of wild-type and plasmid-cured strains: Cysteine showed the spore forming activity, weak activity of aerial mycelium elongation and Thiostrepton productivity; Bacitracin showed the spore forming activity, fairly growth activity on submeriged mycelium and strong elongation activity on areial mycelium; Glutathione showed the spore forming activity. These compounds would enhance the cell metabolism. The inhibiting action of pSA1.1 on the host cells may be depressed by the enhanced metebolism of host cells. The pSA1.1 may code for a protein that can interact in a damage manner with cell membrances.